Updated on 2025/05/13

Information

 

写真a

 
MAKOTO TSUDA
 
Organization
Faculty of Pharmaceutical Sciences Department of Pharmaceutical Health Care and Sciences Professor
Faculty of Pharmaceutical Sciences Drug Discovery and Evolution Center(Concurrent)
School of Pharmaceutical Sciences Department of Clinical Pharmacy(Concurrent)
Graduate School of Pharmaceutical Sciences Department of Clinical Pharmacy(Concurrent)
Graduate School of Pharmaceutical Sciences Department of Medicinal Sciences(Concurrent)
Institute for Advanced Study (Concurrent)
Title
Professor
Contact information
メールアドレス
Profile
Outline of research: Molecular and cellular mechanisms in the peripheral and central nervous system underlying chronic pain and itch focusing on the role of glial cells. Education: Pharmacology, Seminar, Medicine, Neuropharmacology
Homepage
  • http://life-innov.phar.kyushu-u.ac.jp/index-e.html

    Work in my laboratory is primarily directed to elucidating glia-neuron interactions in the spinal cord and brain and to understanding the cellular and molecular mechanisms of pain and itch signaling (in particular pathological chronic pain and itch). Our work employs several cutting-edge genetic tools to manipulate the specific type of cells to determine how identifiable populations of neurons and glial cells contribute to pain and itch behaviors in a causal manner. We also complementally use electrophysiology and cellular functional imaging (in vitro and in vivo) to measure activity of neurons and glial cells. From these studies, we devise strategies for new types of pain and itch relieving medications.

Research Areas

  • Life Science / Pharmacology

Degree

  • Ph.D.

Research History

  • 科学技術振興事業団 特別研究員(国立医薬品食品衛生研究所配属) 医薬品副作用被害救済・研究振興調査機構 派遣研究員(国立医薬品食品衛生研究所配属) 厚生労働省 厚生労働技官(国立医薬品食品衛生研究所配属)   

    科学技術振興事業団 特別研究員(国立医薬品食品衛生研究所配属) 医薬品副作用被害救済・研究振興調査機構 派遣研究員(国立医薬品食品衛生研究所配属) 厚生労働省 厚生労働技官(国立医薬品食品衛生研究所配属)

  • 奈良県立医科大学 非常勤講師 順天堂大学大学院環境医学研究所 客員教授   

Research Interests・Research Keywords

  • Research theme: Research on the mechanisms of pain and itch focusing on neurons and glia in the brain and spinal cord

    Keyword: 脳、脊髄、神経細胞、グリア細胞、痛み、痒み

    Research period: 2014.6

  • Research theme: Molecular and cellular mechanisms of itch

    Keyword: itch, spinal cord, neurons, glia, primary afferent sensory neurons

    Research period: 2012.4 - 2014.5

  • Research theme: Studies on mechanisms underlying the development and maintenance of intractable pain

    Keyword: neuropathic pain, ATP receptors, intracellular signal transduction, glial cells

    Research period: 1999.4 - 2014.6

Awards

  • 令和6年度科学技術分野の文部科学大臣表彰 科学技術賞(研究部門)

    2024.4   文部科学省   グリア細胞を軸とした疼痛の発症と慢性化機序に関する研究

  • 第37回井上学術賞

    2021.2   公益財団法人 井上科学振興財団   グリア細胞による体性感覚(痛みと痒み)制御機構に関する研究

  • 平成19年度日本神経化学会奨励賞(最優秀賞)

    2007.9   日本神経化学会   「脊髄ミクログリアを介する神経因性疼痛の発症維持メカニズム」

  • 平成19年度文部科学大臣表彰若手科学者賞

    2007.4   文部科学省   「生命科学分野における疼痛発症維持機構の研究」

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    「生命科学分野における疼痛発症維持機構の研究」
    癌や糖尿病患者などで見られる神経障害性の慢性疼痛は,モルヒネが著効しない難治性の痛みである。その発症機序は不明で,有効な治療薬もない。従来までの研究は,神経障害性ゆえに,神経細胞での変化のみに注目してきたが,未だ疼痛を制圧するには至っていない。津田誠氏は,難治性疼痛動物モデルの脊髄において,ATP受容体(細胞外ATPの受容体)の一つであるP2X4受容体が,非神経細胞のミクログリアに過剰発現し,その活性化が疼痛の原因であることを世界で初めて発見した。さらに,P2X4受容体刺激後にミクログリアから放出される疼痛因子も特定した。本研究成果は,難治性疼痛におけるミクログリアの重要性を明示したことで,その発症維持機序の解明に大きな前進をもたらし,今後のミクログリア発現分子を標的とした治療薬開発にも繋がると期待される。

  • 第22回日本薬理学会学術奨励賞

    2007.3   日本薬理学会   ATP受容体を介した難治性疼痛発症維持機構

  • Excellent Presentation Award

    2019.11   第6回アジア神経精神薬理学会大会(AsCNP2019)   ポスター発表「Investigation of neuropathic allodynia with sensory and emotional components using an optogenetic approach」に対する賞

  • 日本薬学会学術振興賞

    2019.3   日本薬学会   神経障害性疼痛におけるミクログリア細胞の役割に関する研究

  • 平成25年度九州大学研究活動表彰

    2013.11   九州大学   研究代表者としての競争的研究資金の獲得額が3千万円以上となったため

  • 平成24年度九州大学研究活動表彰

    2012.11   九州大学   研究代表者としての競争的研究資金の獲得額が3千万円以上となったため

  • Best Poster Award

    2012.6   The 7th International Conference of Neurons and Brain Diseases   IRF8 is a critical transcription for transforming microglia into a reactive phenotype

  • 平成23年度九州大学研究活動表彰

    2011.11   九州大学   研究代表者としての競争的研究資金の獲得額が3千万円以上となったため

  • Best Poster Award

    2008.8   The 3rd International Conference of Neurons and Brain Disease   Interferon-γ receptors are required for spinal microglia activation and neuropathic pain after peripheral nerve injury

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Papers

  • Microglial diversity in neuropathic pain Reviewed

    Makoto Tsuda, Takahiro Masuda, Keita Kohno

    Trends in Neurosciences   46 ( 7 )   597 - 610   2023.7   ISSN:0166-2236

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    Authorship:Lead author, Corresponding author   Language:Others   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    Microglia play pivotal roles in controlling CNS functions in diverse physiological and pathological contexts, including neuropathic pain, a chronic pain condition caused by lesions or diseases of the somatosensory nervous system. In this review article, we summarize evidence primarily from basic research on the role of microglia in the development and remission of neuropathic pain. The identification of a subset of microglia that emerged after pain development and that was necessary for remission of neuropathic pain highlights the highly divergent and dynamic nature of microglia in the course of neuropathic pain. Understanding microglial diversity in terms of gene expression, physiological states, and functional roles could lead to new strategies that aid in the diagnosis and management of neuropathic pain, and that may not have been anticipated from the viewpoint of targeting all microglia uniformly.

    DOI: 10.1016/j.tins.2023.05.001

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  • Neuronal pentraxin 2 is required for facilitating excitatory synaptic inputs onto spinal neurons involved in pruriceptive transmission in a model of chronic itch. Reviewed International journal

    Kensho Kanehisa, Keisuke Koga, Sho Maejima, Yuto Shiraishi, Konatsu Asai, Miho Shiratori-Hayashi, Mei-Fang Xiao, Hirotaka Sakamoto, Paul F Worley, Makoto Tsuda

    Nature communications   13 ( 1 )   2367 - 2367   2022.5

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Nature Communications  

    An excitatory neuron subset in the spinal dorsal horn (SDH) that expresses gastrin-releasing peptide receptors (GRPR) is critical for pruriceptive transmission. Here, we show that glutamatergic excitatory inputs onto GRPR+ neurons are facilitated in mouse models of chronic itch. In these models, neuronal pentraxin 2 (NPTX2), an activity-dependent immediate early gene product, is upregulated in the dorsal root ganglion (DRG) neurons. Electron microscopy reveals that NPTX2 is present at presynaptic terminals connected onto postsynaptic GRPR+ neurons. NPTX2-knockout prevents the facilitation of synaptic inputs to GRPR+ neurons, and repetitive scratching behavior. DRG-specific NPTX2 expression rescues the impaired behavioral phenotype in NPTX2-knockout mice. Moreover, ectopic expression of a dominant-negative form of NPTX2 in DRG neurons reduces chronic itch-like behavior in mice. Our findings indicate that the upregulation of NPTX2 expression in DRG neurons contributes to the facilitation of glutamatergic inputs onto GRPR+ neurons under chronic itch-like conditions, providing a potential therapeutic target.

    DOI: 10.1038/s41467-022-30089-x

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  • A spinal microglia population involved in remitting and relapsing neuropathic pain. Reviewed International journal

    Keita Kohno, Ryoji Shirasaka, Kohei Yoshihara, Satsuki Mikuriya, Kaori Tanaka, Keiko Takanami, Kazuhide Inoue, Hirotaka Sakamoto, Yasuyuki Ohkawa, Takahiro Masuda, Makoto Tsuda

    Science (New York, N.Y.)   376 ( 6588 )   86 - 90   2022.4   ISSN:00368075 eISSN:10959203

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:American Association for the Advancement of Science (AAAS)  

    Neuropathic pain is often caused by injury and diseases that affect the somatosensory system. Although pain development has been well studied, pain recovery mechanisms remain largely unknown. Here, we found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury. Nerve-injured mice with spinal CD11c+ microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c+ microglia expressed insulin-like growth factor-1 (IGF1), and interference with IGF1 signaling recapitulated the impairment in pain recovery. In pain-recovered mice, the depletion of CD11c+ microglia or the interruption of IGF1 signaling resulted in a relapse in pain hypersensitivity. Our findings reveal a mechanism for the remission and recurrence of neuropathic pain, providing potential targets for therapeutic strategies.

    DOI: 10.1126/science.abf6805

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  • A subset of spinal dorsal horn interneurons crucial for gating touch-evoked pain-like behavior. Reviewed International journal

    Ryoichi Tashima, Keisuke Koga, Yu Yoshikawa, Misuzu Sekine, Moeka Watanabe, Hidetoshi Tozaki-Saitoh, Hidemasa Furue, Toshiharu Yasaka, Makoto Tsuda

    Proceedings of the National Academy of Sciences of the United States of America   118 ( 3 )   2021.1

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    A cardinal, intractable symptom of neuropathic pain is mechanical allodynia, pain caused by innocuous stimuli via low-threshold mechanoreceptors such as Aβ fibers. However, the mechanism by which Aβ fiber-derived signals are converted to pain remains incompletely understood. Here we identify a subset of inhibitory interneurons in the spinal dorsal horn (SDH) operated by adeno-associated viral vectors incorporating a neuropeptide Y promoter (AAV-NpyP+) and show that specific ablation or silencing of AAV-NpyP+ SDH interneurons converted touch-sensing Aβ fiber-derived signals to morphine-resistant pain-like behavioral responses. AAV-NpyP+ neurons received excitatory inputs from Aβ fibers and transmitted inhibitory GABA signals to lamina I neurons projecting to the brain. In a model of neuropathic pain developed by peripheral nerve injury, AAV-NpyP+ neurons exhibited deeper resting membrane potentials, and their excitation by Aβ fibers was impaired. Conversely, chemogenetic activation of AAV-NpyP+ neurons in nerve-injured rats reversed Aβ fiber-derived neuropathic pain-like behavior that was shown to be morphine-resistant and reduced pathological neuronal activation of superficial SDH including lamina I. These findings suggest that identified inhibitory SDH interneurons that act as a critical brake on conversion of touch-sensing Aβ fiber signals into pain-like behavioral responses. Thus, enhancing activity of these neurons may offer a novel strategy for treating neuropathic allodynia.

    DOI: 10.1073/pnas.2021220118

  • Spinal astrocytes in superficial laminae gate brainstem descending control of mechanosensory hypersensitivity. Reviewed International journal

    Yuta Kohro, Tsuyoshi Matsuda, Kohei Yoshihara, Keita Kohno, Keisuke Koga, Ryuichi Katsuragi, Takaaki Oka, Ryoichi Tashima, Sho Muneta, Takuya Yamane, Shota Okada, Kazuya Momokino, Aogu Furusho, Kenji Hamase, Takumi Oti, Hirotaka Sakamoto, Kenichiro Hayashida, Ryosuke Kobayashi, Takuro Horii, Izuho Hatada, Hidetoshi Tozaki-Saitoh, Katsuhiko Mikoshiba, Verdon Taylor, Kazuhide Inoue, Makoto Tsuda

    Nature neuroscience   23 ( 11 )   1376 - 1387   2020.11

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    Astrocytes are critical regulators of CNS function and are proposed to be heterogeneous in the developing brain and spinal cord. Here we identify a population of astrocytes located in the superficial laminae of the spinal dorsal horn (SDH) in adults that is genetically defined by Hes5. In vivo imaging revealed that noxious stimulation by intraplantar capsaicin injection activated Hes5+ SDH astrocytes via α1A-adrenoceptors (α1A-ARs) through descending noradrenergic signaling from the locus coeruleus. Intrathecal norepinephrine induced mechanical pain hypersensitivity via α1A-ARs in Hes5+ astrocytes, and chemogenetic stimulation of Hes5+ SDH astrocytes was sufficient to produce the hypersensitivity. Furthermore, capsaicin-induced mechanical hypersensitivity was prevented by the inhibition of descending locus coeruleus-noradrenergic signaling onto Hes5+ astrocytes. Moreover, in a model of chronic pain, α1A-ARs in Hes5+ astrocytes were critical regulators for determining an analgesic effect of duloxetine. Our findings identify a superficial SDH-selective astrocyte population that gates descending noradrenergic control of mechanosensory behavior.

    DOI: 10.1038/s41593-020-00713-4

  • Sensitization of spinal itch transmission neurons in a mouse model of chronic itch requires an astrocytic factor Reviewed International journal

    Keisuke Koga, Ryo Yamagata, Keita Kohno, Takuya Yamane, Miho Shiratori-Hayashi, Yuta Kohro, Hidetoshi Tozaki-Saitoh, Makoto Tsuda

    Journal of Allergy and Clinical Immunology   145 ( 1 )   183 - 191.e10   2020.1

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    Background: Chronic itch is a highly debilitating symptom among patients with inflammatory skin diseases. Recent studies have revealed that gastrin-releasing peptide (GRP) and its receptor (gastrin-releasing peptide receptor [GRPR]) in the spinal dorsal horn (SDH) play a central role in itch transmission. Objective: We aimed to investigate whether GRP-GRPR signaling is altered in SDH neurons in a mouse model of chronic itch and to determine the potential mechanisms underlying these alterations. Methods: Patch-clamp recordings from enhanced green fluorescent protein (EGFP)–expressing (GRPR+) SDH neurons were used to examine GRP-GRPR signaling in spinal cord slices obtained from Grpr-EGFP mice. Immunohistochemical, genetic (gene expression and editing through adeno-associated virus vectors), and behavioral approaches were also used for in vivo experiments. Results: We observed potentiation of GRP-evoked excitation in the GRPR+ SDH neurons of mice with contact dermatitis, without concomitant changes in GRPR expression. Interestingly, increases in excitation were attenuated by suppressing the reactive state of SDH astrocytes, which are known to be reactive in patients with chronic itch conditions. Furthermore, CRISPR-Cas9–mediated astrocyte-selective in vivo editing of a gene encoding lipocalin-2 (LCN2), an astrocytic factor implicated in chronic itch, suppressed increases in GRP-induced excitation of GRPR+ neurons, repetitive scratching, and skin damage in mice with contact dermatitis. Moreover, LCN2 potentiated GRP-induced excitation of GRPR+ neurons in normal mice. Conclusion: Our findings indicate that, under chronic itch conditions, the GRP-induced excitability of GRPR+ SDH neurons is enhanced through a non–cell-autonomous mechanism involving LCN2 derived from reactive astrocytes.

  • Role of P2X3 receptors in scratching behavior in mouse models Reviewed International journal

    Shiratori-Hayashi M, Hasegawa A, Toyonaga H, Andoh T, Nakahara T, Kido-Nakahara M, Furue M, Kuraishi Y, Inoue K, Dong X, Tsuda M

    J Allergy Clin Immunol   143 ( 3 )   1252 - 1254.e8   2019.3

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    Authorship:Last author, Corresponding author   Language:Japanese   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaci.2018.10.053

  • Optogenetic activation of non-nociceptive Aβ fibers induces neuropathic pain-like sensory and emotional behaviors after nerve injury in rats. Reviewed International journal

    Tashima R, Koga K, Sekine M, Kanehisa K, Kohro Y, Tominaga K, Matsushita K, Tozaki-Saitoh H, Fukazawa Y, Inoue K, Yawo H, Furue H, Tsuda M

    eNeuro   5   ENEURO.0450-17.2018   2018.2

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1523/ENEURO.0450-17.2018

  • Dorsal horn neurons release extracellular ATP in a VNUT-dependent manner that underlies neuropathic pain Reviewed International journal

    Masuda T et al.

    Nat Commun   7   12529   2016.8

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

  • Bone marrow-derived cells in the population of spinal microglia after peripheral nerve injury Reviewed International journal

    Tashima R et al.

    Sci Rep   6   23701   2016.3

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  • A new minimally-invasive method for microinjection into the mouse spinal dorsal horn Reviewed International journal

    Yuta Kohro et al.

    Sci Rep   5   14306   2015.9

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  • STAT3-dependent reactive astrogliosis in the spinal dorsal horn underlies chronic itch Reviewed International journal

    Miho Shiatori-Hayashi et al.

    NATURE MEDICINE   21 ( 8 )   927 - 931   2015.8

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    Chronic itch is an intractable symptom of inflammatory skin diseases, such as atopic and contact dermatitis. Recent studies have revealed neuronal pathways selective for itch, but the mechanisms by which itch turns into a pathological chronic state are poorly understood. Using mouse models of atopic and contact dermatitis, we demonstrate a long-term reactive state of astrocytes in the dorsal horn of the spinal segments that corresponds to lesioned, itchy skin. We found that reactive astrogliosis depended on the activation of signal transducer and activator of transcription 3 (STAT3). Conditional disruption of astrocytic STAT3 suppressed chronic itch, and pharmacological inhibition of spinal STAT3 ameliorated the fully developed chronic itch. Mice with atopic dermatitis exhibited an increase in scratching elicited by intrathecal administration of the itch-inducer gastrin-releasing peptide (GRP), and this enhancement was normalized by suppressing STAT3-mediated reactive astrogliosis. Moreover, we identified lipocalin-2 (LCN2) as an astrocytic STAT3-dependent upregulated factor that was crucial for chronic itch, and we demonstrated that intrathecal administration of LCN2 to normal mice increased spinal GRP-evoked scratching. Our findings indicate that STAT3-dependent reactive astrocytes act as critical amplifiers of itching through a mechanism involving the enhancement of spinal itch signals by LCN2, thereby providing a previously unrecognized target for treating chronic itch.

    DOI: 10.1038/nm.3912

  • Transcription factor IRF5 drives P2X4R+-reactive microglia gating neuropathic pain. Reviewed International journal

    Masuda Takahiro et al.

    Nat Commun   5   3771   2014.5

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    神経のダメージで発症する慢性的な痛み(神経障害性疼痛)の原因タンパク質として「IRF5」を突き止めました。IRF5は、神経の損傷後に脳・脊髄の免疫細胞であるミクログリアで増え、IRF5欠損マウスでは痛みが弱くなっていました。さらに、2003年にP2X4受容体タンパク質のミクログリアでの増加が神経障害性疼痛に重要であることを英国科学誌Natureで発表していますが、今回見つかったIRF5がP2X4受容体を増やす実行役であることも明らかにしました。この研究成果は、慢性疼痛メカニズムの解明へ向けた大きな前進となり、痛みを緩和する治療薬の開発に応用できることが期待されます(Nature Communications誌掲載)。

  • IRF8 Is a Critical Transcription Factor for Transforming Microglia into a Reactive Phenotype Reviewed International journal

    Masuda Takahiro, TSUDA MAKOTO, Ryohei Yoshinaga, Hidetoshi Saitoh, Keiko Ozato, Tomohiko Tamura, Kazuhide Inoue

    CELL REPORTS   1 ( 4 )   334 - 340   2012.4

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    神経のダメージで発症する慢性的な激しい痛み(神経障害性疼痛)の原因タンパク質として「IRF8」を突き止めました。神経の損傷後,IRF8は脳・脊髄の免疫細胞と呼ばれる「ミクログリア」だけで劇的に増えており,同細胞の過度な活性化状態をつくりだして激しい痛みを引き起こすことを明らかにしました。また,IRF8は中枢神経においてミクログリア特異的に発現する転写因子として世界初の例であり,他の神経疾患においてもミクログリアの活性化が報告されていることから,他の領域にも本成果が波及することが期待できる。この研究成果は,慢性疼痛メカニズムの解明へ向けた大きな前進となり,痛みを緩和する治療薬の開発に応用できることが期待されます(Cell Reports誌掲載)。

    DOI: 10.1016/j.celrep.2012.02.014

  • Neuronal CCL21 up-regulates microglia P2X4 expression and initiates neuropathic pain development. Reviewed International journal

    Biber K*, Tsuda M*, Tozaki-Saitoh H*, Tsukamoto K, Toyomitsu E, Masuda T, Boddeke H, Inoue K. (*equal contributors)

    EMBO J   30 ( 9 )   2011.5

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  • JAK-STAT3 pathway regulates spinal astrocyte proliferation and neuropathic pain maintenance in rats. Reviewed International journal

    Tsuda M, Kohro Y, Yano T, Tsujikawa T, Kitano J, Tozaki-Saitoh H, Koyanagi S, Ohdo S, Ji RR, Salter MW, Inoue K

    Brain   134 ( 4 )   2011.4

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  • Mechanisms underlying fibronectin-induced up-regulation of P2X4R expression in microglia: distinct roles of PI3K-Akt and MEK-ERK signalling pathways Reviewed International journal

    Tsuda M, Toyomitsu E, Kometani M, Tozaki-Saitoh H, Inoue K

    J Cell Mol Med   13 ( 9b )   2009.9

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  • Behavioral phenotypes of mice lacking purinergic P2X4 receptors in acute and chronic pain assays Reviewed International journal

    Tsuda M, Kuboyama K, Inoue T, Nagata K, Tozaki-Saitoh H, Inoue K

    Mol Pain   5   2009.6

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  • IFN-gamma receptor signaling mediates spinal microglia activation driving neuropathic pain Reviewed International journal

    Tsuda M, Masuda T, Kitano J, Shimoyama H, Tozaki-Saitoh H, Inoue K

    Proc Natl Acad Sci U S A   106 ( 19 )   2009.5

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  • P2Y12 receptors in spinal microglia are required for neuropathic pain after peripheral nerve injury Reviewed International journal

    Tozaki-Saitoh H, Tsuda M, Miyata H, Ueda K, Kohsaka S, Inoue K

    J Neurosci 28: 4949-4956 (2008)   2008.5

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  • Fibronectin/integrin system is involved in P2X(4) receptor upregulation in the spinal cord and neuropathic pain after nerve injury Reviewed International journal

    Tsuda M, Toyomitsu E, Komatsu T, Masuda T, Kunifusa E, Nasu-Tada K, Koizumi S, Yamamoto K, Ando J, Inoue K

    Glia 56: 579-585 (2008)   2008.4

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  • UDP acting at P2Y(6) receptors is a mediator of microglial phagocytosis. Reviewed International journal

    Koizumi S, Shigemoto-Mogami Y, Nasu-Tada K, Shinozaki Y, Ohsawa K, Tsuda M, Joshi BV, Jacobson KA, Kohsaka S, Inoue K.

    Nature. 446: 1091-1095 (2007)   2007.4

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  • BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain. Reviewed International journal

    Coull JA, Beggs S, Boudreau D, Boivin D, Tsuda M, Inoue K, Gravel C, Salter MW, De Koninck Y.

    Nature. 2005 Dec 15;438(7070):1017-21.   438 ( 7070 )   1017 - 1021   2005.12

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/nature04223

  • Activation of p38 mitogen-activated protein kinase in spinal hyperactive microglia contributes to pain hypersensitivity following peripheral nerve injury. Reviewed International journal

    Tsuda M, Mizokoshi A, Shigemoto-Mogami Y, Koizumi S, Inoue K.

    Glia. 2004 Jan 1;45(1):89-95.   45 ( 1 )   89 - 95   2004.1

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/glia.10308

  • P2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury. Reviewed International journal

    Tsuda M, Shigemoto-Mogami Y, Koizumi S, Mizokoshi A, Kohsaka S, Salter MW, Inoue K. Related Articles, Links

    Nature. 2003 Aug 14;424(6950):778-83.   424 ( 6950 )   778 - 783   2003.8

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  • Mechanical allodynia caused by intraplantar injection of P2X receptor agonist in rats: involvement of heteromeric P2X2/3 receptor signaling in capsaicin-insensitive primary afferent neurons. Reviewed International journal

    Tsuda M, Koizumi S, Kita A, Shigemoto Y, Ueno S, Inoue K.

    J Neurosci. 2000 Aug 1;20(15):RC90.   20 ( 15 )   2000.8

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  • Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders

    Fuma K., Iitani Y., Imai K., Ushida T., Tano S., Yoshida K., Yokoi A., Miki R., Kidokoro H., Sato Y., Hara Y., Ogi T., Nomaki K., Tsuda M., Komine O., Yamanaka K., Kajiyama H., Kotani T.

    Communications Biology   8 ( 1 )   75   2025.12

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    Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopmental disorders in offspring. Our previous study identified neurodevelopmental impairments in an MIA mouse model mimicking HCA. Thus, this study investigated the role of CD11c+ microglia, key contributors to myelination through IGF-1 production, in this pathology. In the mouse model, the CD11c+ microglial population was significantly lower in the MIA group than in the control group on postnatal day 3 (PN3d). Furthermore, myelination-related protein levels significantly decreased in the MIA group at PN8d. In humans, preterm infants with HCA exhibited higher IL-6 and IL-17A cord-serum levels and lower IGF-1 levels than those without HCA, followed by a higher incidence of delayed myelination on magnetic resonance imaging at the term-equivalent age. In silico analysis revealed that the transient induction of CD11c+ microglia during early development occurred similarly in mice and humans. Notably, a lack of high CD11c+ microglial population has been observed in children with neurodevelopmental disorders. This study reports impaired induction of CD11c+ microglia during postnatal development in a mouse model of MIA associated with delayed myelination. Our findings may inform strategies for improving outcomes in infants with HCA. (Figure presented.)

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  • Neuron-microglia interactions modulating neuropathic pain.

    Kohno K, Tsuda M

    International immunology   2025.4   ISSN:0953-8178

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  • Spinal dorsal horn neurons involved in the alleviating effects of cannabinoid receptor agonists on neuropathic allodynia-like behaviors in rats

    Sueto D., I E., Onishi A., Tsuda M.

    Journal of Pharmacological Sciences   157 ( 4 )   253 - 260   2025.4   ISSN:13478613

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    Mechanical allodynia, the pain caused by innocuous tactile stimuli, is a hallmark symptom of neuropathic pain that is often resistant to currently available treatments. Cannabinoids are widely used for pain management; however, their therapeutic mechanisms for neuropathic mechanical allodynia remain unclear. Using transgenic rats that enable to optogenetically stimulate touch-sensing Aβ fibers in the skin, we found that the intrathecal administration of the synthetic cannabinoid, WIN 55,212-2, alleviated the Aβ fiber-derived neuropathic allodynia. Furthermore, we injected adeno-associated virus vectors incorporating the rat cannabinoid receptor 1 (CB1 receptor) (encoded by Cnr1) promoter and tdTomato or short hairpin RNA targeting the CB1 receptor into the spinal dorsal horn (SDH) and demonstrated that the conditional knockdown of CB1 receptors in Cnr1+ SDH neurons attenuates the anti-allodynic effects of intrathecally administered WIN 55,212-2. Electrophysiological analysis revealed that Cnr1+ SDH neurons received excitatory synaptic inputs from the primary afferent Aβ fibers. Collectively, our results suggest that the CB1 receptors in Cnr1+ SDH neurons are molecular and cellular targets of intrathecal WIN 55,212-2 to alleviate neuropathic allodynia.

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  • Descending locus coeruleus noradrenergic signaling to spinal astrocyte subset is required for stress-induced pain facilitation

    Riku Kawanabe-Kobayashi, Sawako Uchiyama, Kohei Yoshihara, Daiki Kojima, Thomas McHugh, Izuho Hatada, Ko Matsui, Kenji F Tanaka, Makoto Tsuda

    2025.3

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    It is known that stress powerfully alters pain, but its underlying mechanisms remain elusive. Here, we identified a circuit, locus coeruleus descending noradrenergic neurons projecting to the spinal dorsal horn (LC→SDH-NA neurons), that is activated by acute exposure to restraint stress and is required for stress-induced mechanical pain hypersensitivity in mice. Interestingly, the primary target of spinal NA released from descending LC→SDH-NAergic terminals causing the stress-induced pain hypersensitivity was α1A-adrenaline receptors (α1ARs) in Hes5-positive (Hes5+) astrocytes located in the SDH, an astrocyte subset that has an ability to induce pain sensitization. Furthermore, activation of Hes5+ astrocytes reduced activity of SDH-inhibitory neurons (SDH-INs) that have an inhibitory role in pain processing. This astrocytic reduction of IN activity was canceled by an A1-adenosine receptor (A1R)-knockdown in SDH-INs, and the A1R-knockdown suppressed pain hypersensitivity caused by acute restraint stress. Therefore, our findings suggest that LC→SDH-NA neuronal signaling to Hes5+ SDH astrocytes and subsequent astrocytic reduction of SDH-IN activity are essential for pain facilitation caused by stress.

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  • Pharmacological Profile of NCP-322, a Novel G Protein-Coupled Receptor 119 Agonist, as an Orally Active Therapeutic Agent for Type 2 Diabetes Mellitus

    Nakamura H., Endo T., Tsuda M.

    Biological and Pharmaceutical Bulletin   48 ( 1 )   65 - 74   2025.1   ISSN:09186158

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    Pharmacological activation of G protein-coupled receptor 119 (GPR119) produces pleiotropic beneficial effects, including the promotion of insulin secretion from pancreatic β-cells, enhancement of glucagon-like peptide (GLP)-1 secretion from intestinal L cells, glucose-dependent insulin secretion, and food intake and body weight gain suppression. Thus, GPR119 has attracted attention as a promising new target for type 2 diabetes mellitus (T2DM) treatment. Here, we identified a new small GPR119 agonist, NCP-322. This compound showed potent enhancing effects on insulin and GLP-1 secretion, which played a role in pancreatic β-cells and intestinal L cells. In the oral glucose tolerance test, NCP-322 administration reduced glycemic excursions that were only exhibited during hyperglycemia. Furthermore, NCP-322 administration did not induce hypoglycemia, the main side effect of antidiabetic drugs. These results suggest the promising therapeutic potential of NCP-322 for T2DM treatment.

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  • IRF8 and MAFB drive distinct transcriptional machineries in different resident macrophages of the central nervous system Reviewed

    Ayato Yamasaki, Iroha Imanishi, Kaori Tanaka, Yasuyuki Ohkawa, Makoto Tsuda, Takahiro Masuda

    Communications Biology   7 ( 1 )   896   2024.12

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    The central nervous system (CNS) includes anatomically distinct macrophage populations including parenchyma microglia and CNS-associated macrophages (CAMs) localized at the interfaces like meninges and perivascular space, which play specialized roles for the maintenance of the CNS homeostasis with the help of precisely controlled gene expressions. However, the transcriptional machinery that determines their cell-type specific states of microglia and CAMs remains poorly understood. Here we show, by myeloid cell-specific deletion of transcription factors, IRF8 and MAFB, that both adult microglia and CAMs utilize IRF8 to maintain their core gene signatures, although the genes altered by IRF8 deletion are different in the two macrophage populations. By contrast, MAFB deficiency robustly affected the gene expression profile of adult microglia, whereas CAMs are almost independent of MAFB. Our data suggest that distinct transcriptional machineries regulate different macrophages in the CNS.

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  • MrgprA3+ Primary Sensory Neurons Mediate Acute Allergic Itch Responses in Atopic Dermatitis Model Mice Reviewed

    Kyoko Fujii, Ryosuke Miyagawa, Rina Tanaka, Michiko Saito, Satoshi Tanaka, Miho Shiratori-Hayashi, Makoto Tsuda, Xinzhong Dong, Masanori Fujii

    Biological and Pharmaceutical Bulletin   47 ( 10 )   1624 - 1630   2024.10   ISSN:0918-6158 eISSN:1347-5215

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    Itch is a prominent symptom of atopic dermatitis (AD). However, the underlying mechanism remains complex and has not yet been fully elucidated. Mas-related G protein-coupled receptor A3 (MrgprA3) has emerged attention as a marker of primary sensory neurons that specifically transmit itch signals; however, its involvement in AD-related itch has not been extensively explored. In this study, we developed an AD itch mouse model by repeatedly applying house dust mite (HDM) extract to barrier-impaired skin via a special diet. To clarify the role of MrgprA3+ neurons in itch behavior in our AD model, we adopted a toxin receptor-mediated cell knockout strategy using transgenic mice in which the diphtheria toxin receptor (DTR) gene was placed under the control of the Mrgpra3 promoter. When the HDM extract was repeatedly applied to the face and back skin of special diet-fed mice, the mice exhibited AD-like dry and eczematous skin lesions accompanied by three types of itch-related behaviors:1) spontaneous scratching, 2) acute scratching after antigen challenge, and 3) light touch-evoked scratching. Upon diphtheria toxin administration, substantial depletion of DTR+/MrgprA3+ neurons was observed in the dorsal root ganglion. Ablation of MrgprA3+ neurons suppressed acute itch responses after HDM application, whereas spontaneous and touch-evoked itch behaviors remained unaffected. Our findings unequivocally demonstrate that in our AD model, MrgprA3+ primary sensory neurons mediate acute allergic itch responses, whereas these neurons are not involved in spontaneous itch or alloknesis.

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  • Disease-relevant upregulation of P2Y1 receptor in astrocytes enhances neuronal excitability via IGFBP2 Reviewed

    Eiji Shigetomi, Hideaki Suzuki, Yukiho J. Hirayama, Fumikazu Sano, Yuki Nagai, Kohei Yoshihara, Keisuke Koga, Toru Tateoka, Hideyuki Yoshioka, Youichi Shinozaki, Hiroyuki Kinouchi, Kenji F. Tanaka, Haruhiko Bito, Makoto Tsuda, Schuichi Koizumi

    Nature Communications   15 ( 1 )   6525   2024.8   eISSN:2041-1723

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    Reactive astrocytes play a pivotal role in the pathogenesis of neurological diseases; however, their functional phenotype and the downstream molecules by which they modify disease pathogenesis remain unclear. Here, we genetically increase P2Y<sub>1</sub> receptor (P2Y1R) expression, which is upregulated in reactive astrocytes in several neurological diseases, in astrocytes of male mice to explore its function and the downstream molecule. This astrocyte-specific P2Y1R overexpression causes neuronal hyperexcitability by increasing both astrocytic and neuronal Ca<sup>2+</sup> signals. We identify insulin-like growth factor-binding protein 2 (IGFBP2) as a downstream molecule of P2Y1R in astrocytes; IGFBP2 acts as an excitatory signal to cause neuronal excitation. In neurological disease models of epilepsy and stroke, reactive astrocytes upregulate P2Y1R and increase IGFBP2. The present findings identify a mechanism underlying astrocyte-driven neuronal hyperexcitability, which is likely to be shared by several neurological disorders, providing insights that might be relevant for intervention in diverse neurological disorders.

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  • A method for selective and efficient isolation of gray matter astrocytes from the spinal cord of adult mice

    Iwasaki Ryoma, Kohro Yuta, Tsuda Makoto

    Molecular Brain   17   25   2024.5   eISSN:17566606

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    A growing body of evidence indicates intra- and inter-regional heterogeneity of astrocytes in the brain. However, because of a lack of an efficient method for isolating astrocytes from the spinal cord, little is known about how much spinal cord astrocytes are heterogeneous in adult mice. In this study, we developed a new method for isolating spinal astrocytes from adult mice using a cold-active protease from Bacillus licheniformis with an astrocyte cell surface antigen-2 (ACSA-2) antibody. Using fluorescence-activated cell sorting, isolated spinal ACSA-2^+ cells were divided into two distinct populations, ACSA-2^<high> and ACSA-2^<low>. By analyzing the expression of cell-type marker genes, the ACSA-2^<high> and ACSA-2^<low> populations were identified as astrocytes and ependymal cells, respectively. Furthermore, ACSA-2^<high> cells had mRNAs encoding genes that were abundantly expressed in the gray matter (GM) but not white matter astrocytes. By optimizing enzymatic isolation procedures, the yield of GM astrocytes also increased. Therefore, our newly established method enabled the selective and efficient isolation of GM astrocytes from the spinal cord of adult mice and may be useful for bulk- or single-cell RNA-sequencing under physiological and pathological conditions.

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  • A method for selective and efficient isolation of gray matter astrocytes from the spinal cord of adult mice. Reviewed International journal

    Ryoma Iwasaki, Yuta Kohro, Makoto Tsuda

    Molecular brain   17 ( 1 )   25 - 25   2024.5

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    A growing body of evidence indicates intra- and inter-regional heterogeneity of astrocytes in the brain. However, because of a lack of an efficient method for isolating astrocytes from the spinal cord, little is known about how much spinal cord astrocytes are heterogeneous in adult mice. In this study, we developed a new method for isolating spinal astrocytes from adult mice using a cold-active protease from Bacillus licheniformis with an astrocyte cell surface antigen-2 (ACSA-2) antibody. Using fluorescence-activated cell sorting, isolated spinal ACSA-2+ cells were divided into two distinct populations, ACSA-2high and ACSA-2low. By analyzing the expression of cell-type marker genes, the ACSA-2high and ACSA-2low populations were identified as astrocytes and ependymal cells, respectively. Furthermore, ACSA-2high cells had mRNAs encoding genes that were abundantly expressed in the gray matter (GM) but not white matter astrocytes. By optimizing enzymatic isolation procedures, the yield of GM astrocytes also increased. Therefore, our newly established method enabled the selective and efficient isolation of GM astrocytes from the spinal cord of adult mice and may be useful for bulk- or single-cell RNA-sequencing under physiological and pathological conditions.

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  • Spatiotemporal dynamics of the CD11c+ microglial population in the mouse brain and spinal cord from developmental to adult stages. Reviewed International journal

    Kohei Nomaki, Risako Fujikawa, Takahiro Masuda, Makoto Tsuda

    Molecular brain   17 ( 1 )   24 - 24   2024.5

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    CD11c-positive (CD11c+) microglia have attracted considerable attention because of their potential implications in central nervous system (CNS) development, homeostasis, and disease. However, the spatiotemporal dynamics of the proportion of CD11c+ microglia in individual CNS regions are poorly understood. Here, we investigated the proportion of CD11c+ microglia in six CNS regions (forebrain, olfactory bulb, diencephalon/midbrain, cerebellum, pons/medulla, and spinal cord) from the developmental to adult stages by flow cytometry and immunohistochemical analyses using a CD11c reporter transgenic mouse line, Itgax-Venus. We found that the proportion of CD11c+ microglia in total microglia varied between CNS regions during postnatal development. Specifically, the proportion was high in the olfactory bulb and cerebellum at postnatal day P(4) and P7, respectively, and approximately half of the total microglia were CD11c+. The proportion declined sharply in all regions to P14, and the low percentage persisted over P56. In the spinal cord, the proportion of CD11c+ microglia was also high at P4 and declined to P14, but increased again at P21 and thereafter. Interestingly, the distribution pattern of CD11c+ microglia in the spinal cord markedly changed from gray matter at P4 to white matter at P21. Collectively, our findings reveal the differences in the spatiotemporal dynamics of the proportion of CD11c+ microglia among CNS regions from early development to adult stages in normal mice. These findings improve our understanding of the nature of microglial heterogeneity and its dynamics in the CNS.

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  • Laminar-selective spinal astrocyte population capable of converting tactile information into nociceptive in rats Reviewed

    Sueto D., Onishi A., I E., Yoshikawa Y., Tsuda M.

    Journal of Pharmacological Sciences   154 ( 4 )   312 - 315   2024.4   ISSN:13478613

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    We previously identified a spinal astrocyte population that expresses hairy and enhancer of split 5 (Hes5) and is selectively present in superficial laminae in mice. However, it was unclear whether such astrocyte heterogeneity is commonly observed across species. Using adeno-associated viral (AAV) vectors incorporating a rat Hes5 promotor (AAV-Hes5P), we found that AAV-Hes5P-captured astrocytes were selectively located in the superficial laminae in rats. Furthermore, activation of AAV-Hes5P+ astrocytes elicited allodynia-like behavior and increased c-FOS+ cells in the superficial laminae. Thus, laminar-selective Hes5+ astrocytes are conserved beyond species and have the capability to convert tactile information to nociceptive.

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  • Anterior cingulate cross-hemispheric inhibition via the claustrum resolves painful sensory conflict Reviewed

    Keisuke Koga, Kenta Kobayashi, Makoto Tsuda, Anthony E. Pickering, Hidemasa Furue

    Communications Biology   7 ( 1 )   330   2024.3   eISSN:2399-3642

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    The anterior cingulate cortex (ACC) responds to noxious and innocuous sensory inputs, and integrates them to coordinate appropriate behavioral reactions. However, the role of the projections of ACC neurons to subcortical areas and their influence on sensory processing are not fully investigated. Here, we identified that ACC neurons projecting to the contralateral claustrum (ACC<sup>→contraCLA</sup>) preferentially respond to contralateral mechanical sensory stimulation. These sensory responses were enhanced during attending behavior. Optogenetic activation of ACC<sup>→contraCLA</sup> neurons silenced pyramidal neurons in the contralateral ACC by recruiting local circuit fast-spiking interneuron activation via an excitatory relay in the CLA. This circuit activation suppressed withdrawal behavior to mechanical stimuli ipsilateral to the ACC<sup>→contraCLA</sup> neurons. Chemogenetic silencing showed that the cross-hemispheric circuit has an important role in the suppression of contralateral nociceptive behavior during sensory-driven attending behavior. Our findings identify a cross-hemispheric cortical-subcortical-cortical arc allowing the brain to give attentional priority to competing innocuous and noxious inputs.

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  • 特集 アロスタシス-ホメオスタシスを超えて 慢性疼痛とアロスタシス-グリア細胞の役割

    津田 誠

    BRAIN and NERVE   75 ( 11 )   1225 - 1229   2023.11   ISSN:18816096 eISSN:13448129

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  • Neuropathic pain decoded by microglial heterogeneity

    Tsuda Makoto, Kohno Keita

    Folia Pharmacologica Japonica   158 ( 5 )   362 - 366   2023.9   ISSN:00155691 eISSN:13478397

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    <p>Lesion or diseases affecting the somatosensory system causes neuropathic pain, a debilitating chronic pain condition. Previous studies using its experimental models have demonstrated the critical contribution of microglia to the development of neuropathic pain. Upon sensing nerve damage, spinal cord microglia alter their morphology, gene expression and function, which lead to an increase in the excitability of pain-transmission neural pathway, causing the pain onset. Recently, newly identified CD11c-positive microglia as a subset that increases during the remission phase of neuropathic pain has been shown to be required for spontaneous remission of neuropathic pain and to play an important role in maintaining the remission state. Thus, these findings suggest that the functions and roles of microglia under neuropathic pain conditions are not one-dimensional but change during the onset, maintenance, and remission phases, and they also provide a clue to establish a new strategy to decipher neuropathic pain and other neurological diseases from the heterogeneity of microglia.</p>

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  • Macrophages play a leading role in determining the direction of astrocytic migration in spinal cord injury via ADP-P2Y1R axis. Reviewed International journal

    Gentaro Ono, Kazu Kobayakawa, Hirokazu Saiwai, Tetsuya Tamaru, Hirotaka Iura, Yohei Haruta, Kazuki Kitade, Keiichiro Iida, Kenichi Kawaguchi, Yoshihiro Matsumoto, Makoto Tsuda, Tomohiko Tamura, Keiko Ozato, Kazuhide Inoue, Dai-Jiro Konno, Takeshi Maeda, Seiji Okada, Yasuharu Nakashima

    Scientific reports   13 ( 1 )   11177 - 11177   2023.7

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    After spinal cord injury (SCI), inflammatory cells such as macrophages infiltrate the injured area, and astrocytes migrate, forming a glial scar around macrophages. The glial scar inhibits axonal regeneration, resulting in significant permanent disability. However, the mechanism through which glial scar-forming astrocytes migrate to the injury site has not been clarified. Here we show that migrating macrophages attract reactive astrocytes toward the center of the lesion after SCI. Chimeric mice with bone marrow lacking IRF8, which controls macrophage centripetal migration after SCI, showed widely scattered macrophages in the injured spinal cord with the formation of a huge glial scar around the macrophages. To determine whether astrocytes or macrophages play a leading role in determining the directions of migration, we generated chimeric mice with reactive astrocyte-specific Socs3-/- mice, which showed enhanced astrocyte migration, and bone marrow from IRF8-/- mice. In this mouse model, macrophages were widely scattered, and a huge glial scar was formed around the macrophages as in wild-type mice that were transplanted with IRF8-/- bone marrow. In addition, we revealed that macrophage-secreted ATP-derived ADP attracts astrocytes via the P2Y1 receptor. Our findings revealed a mechanism through which migrating macrophages attract astrocytes and affect the pathophysiology and outcome after SCI.

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  • The Functions and Phenotypes of Microglia in Alzheimer’s Disease Reviewed

    Fujikawa R., Tsuda M.

    Cells   12 ( 8 )   1207   2023.4   eISSN:20734409

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    Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease worldwide, but therapeutic strategies to slow down AD pathology and symptoms have not yet been successful. While attention has been focused on neurodegeneration in AD pathogenesis, recent decades have provided evidence of the importance of microglia, and resident immune cells in the central nervous system. In addition, new technologies, including single-cell RNA sequencing, have revealed heterogeneous cell states of microglia in AD. In this review, we systematically summarize the microglial response to amyloid-β and tau tangles, and the risk factor genes expressed in microglia. Furthermore, we discuss the characteristics of protective microglia that appear during AD pathology and the relationship between AD and microglia-induced inflammation during chronic pain. Understanding the diverse roles of microglia will help identify new therapeutic strategies for AD.

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  • Voltage-gated calcium channel subunit α2δ-1 in spinal dorsal horn neurons contributes to aberrant excitatory synaptic transmission and mechanical hypersensitivity after peripheral nerve injury Reviewed

    Keisuke Koga, Kenta Kobayashi, Makoto Tsuda, Kazufumi Kubota, Yutaka Kitano, Hidemasa Furue

    Frontiers in Molecular Neuroscience   16   1099925   2023.3   ISSN:16625099 eISSN:1662-5099

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    Neuropathic pain, an intractable pain symptom that occurs after nerve damage, is caused by the aberrant excitability of spinal dorsal horn (SDH) neurons. Gabapentinoids, the most commonly used drugs for neuropathic pain, inhibit spinal calcium-mediated neurotransmitter release by binding to α<sub>2</sub>δ-1, a subunit of voltage-gated calcium channels, and alleviate neuropathic pain. However, the exact contribution of α<sub>2</sub>δ-1 expressed in SDH neurons to the altered synaptic transmission and mechanical hypersensitivity following nerve injury is not fully understood. In this study, we investigated which types of SDH neurons express α<sub>2</sub>δ-1 and how α<sub>2</sub>δ-1 in SDH neurons contributes to the mechanical hypersensitivity and altered spinal synaptic transmission after nerve injury. Using in situ hybridization technique, we found that Cacna2d1, mRNA coding α<sub>2</sub>δ-1, was mainly colocalized with Slc17a6, an excitatory neuronal marker, but not with Slc32a1, an inhibitory neuronal marker in the SDH. To investigate the role of α<sub>2</sub>δ-1 in SDH neurons, we used clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system and showed that SDH neuron-specific ablation of Cacna2d1 alleviated mechanical hypersensitivity following nerve injury. We further found that excitatory post-synaptic responses evoked by electrical stimulation applied to the SDH were significantly enhanced after nerve injury, and that these enhanced responses were significantly decreased by application of mirogabalin, a potent α<sub>2</sub>δ-1 inhibitor, and by SDH neuron-specific ablation of Cacna2d1. These results suggest that α<sub>2</sub>δ-1 expressed in SDH excitatory neurons facilitates spinal nociceptive synaptic transmission and contributes to the development of mechanical hypersensitivity after nerve injury.

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  • GPR55 contributes to neutrophil recruitment and mechanical pain induction after spinal cord compression in mice. Reviewed International journal

    Teruaki Ono, Tomohiro Yamashita, Ryota Kano, Mariko Inoue, Shota Okada, Koki Kano, Schuichi Koizumi, Kazuhisa Iwabuchi, Yoshio Hirabayashi, Ichiro Matsuo, Yasuharu Nakashima, Hiroyuki Kamiguchi, Yuta Kohro, Makoto Tsuda

    Brain, behavior, and immunity   110   276 - 287   2023.3   ISSN:08891591

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    Pain transmission and processing in the nervous system are modulated by various biologically active substances, including lysophospholipids, through direct and indirect actions on the somatosensory pathway. Lysophosphatidylglucoside (LysoPtdGlc) was recently identified as a structurally unique lysophospholipid that exerts biological actions via the G protein-coupled receptor GPR55. Here, we demonstrated that GPR55-knockout (KO) mice show impaired induction of mechanical pain hypersensitivity in a model of spinal cord compression (SCC) without the same change in the models of peripheral tissue inflammation and peripheral nerve injury. Among these models, only SCC recruited peripheral inflammatory cells (neutrophils, monocytes/macrophages, and CD3+ T-cells) in the spinal dorsal horn (SDH), and GPR55-KO blunted these recruitments. Neutrophils were the first cells recruited to the SDH, and their depletion suppressed the induction of SCC-induced mechanical hypersensitivity and inflammatory responses in compressed SDH. Furthermore, we found that PtdGlc was present in the SDH and that intrathecal administration of an inhibitor of secretory phospholipase A2 (an enzyme required for producing LysoPtdGlc from PtdGlc) reduced neutrophil recruitment to compressed SDH and suppressed pain induction. Finally, by screening compounds from a chemical library, we identified auranofin as a clinically used drug with an inhibitory effect on mouse and human GPR55. Systemically administered auranofin to mice with SCC effectively suppressed spinal neutrophil infiltration and pain hypersensitivity. These results suggest that GPR55 signaling contributes to the induction of inflammatory responses and chronic pain after SCC via the recruitment of neutrophils and may provide a new target for reducing pain induction after spinal cord compression, such as spinal canal stenosis.

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  • IP3R1-dependent astrocyte calcium signaling in chronic itch Reviewed

    Miho Shiratori-Hayashi, Makoto Tsuda

    Neuroscience Research   187   40 - 44   2023.2   ISSN:0168-0102

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    Astrocytes, the most abundant type of glial cell, are electrically non-excitable cells that use intracellular calcium (Ca2+) for functional regulation. Changes in intracellular Ca2+ concentration play important roles in the central nervous system (CNS), as they are involved in the release of gliotransmitters and the control of extracellular ion concentrations, thereby affecting the regulation of neuronal excitability, CNS homeostasis, and behavior. Intracellular calcium mobilization in astrocytes is known to be mediated via inositol 1,4,5-trisphosphate receptors (IP3Rs), particularly IP3R2, and its association with CNS pathogenesis has been widely reported. In addition, the existence of IP3R2-independent calcium signaling has recently been postulated; however, the detailed mechanisms and its role in astrocyte functions and CNS pathogenesis are still poorly understood. In this paper, we describe the putative mechanisms underlying IP3R1-dependent calcium signaling in astrocytes and its effects on the reactive state, compare this signaling with IP3R2-dependent calcium signaling, and discuss its contribution to chronic itch-like behavior.

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  • Macrophages play a leading role in determining the direction of astrocytic migration in spinal cord injury via ADP-P2Y1R axis. Reviewed International journal

    Gentaro Ono, Kazu Kobayakawa, Hirokazu Saiwai, Tetsuya Tamaru, Hirotaka Iura, Yohei Haruta, Kazuki Kitade, Kei-Ichiro Iida, Ken-Ichi Kawaguchi, Yoshihiro Matsumoto, Makoto Tsuda, Tomohiko Tamura, Keiko Ozato, Kazuhide Inoue, Dai-Jiro Konno, Takeshi Maeda, Seiji Okada, Yasuharu Nakashima

    Research square   2023.1

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    After spinal cord injury (SCI), inflammatory cells such as macrophages infiltrate the injured area, and astrocytes migrate, forming a glial scar around macrophages. The glial scar inhibits axonal regeneration, resulting in significant permanent disability. However, the mechanism by which glial scar-forming astrocytes migrate to the injury site has not been clarified. Here we show that migrating macrophages attract reactive astrocytes toward the center of the lesion after SCI. Chimeric mice with bone marrow lacking IRF8, which controls macrophage centripetal migration after SCI, showed widely scattered macrophages in injured spinal cord with the formation of a huge glial scar around the macrophages. To determine whether astrocytes or macrophages play a leading role in determining the directions of migration, we generated chimeric mice with reactive astrocyte-specific Socs3 -/- mice, which showed enhanced astrocyte migration, and bone marrow from IRF8 -/- mice. In this mouse model, macrophages were widely scattered, and a huge glial scar was formed around the macrophages as in wild-type mice that were transplanted with IRF8 -/ bone marrow. In addition, we revealed that macrophage-secreted ATP-derived ADP attracts astrocytes via the P2Y1 receptor. Our findings revealed a mechanism in which migrating macrophages attracted astrocytes and affected the pathophysiology and outcome after SCI.

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  • Identification of Spinal Inhibitory Interneurons Required for Attenuating Effect of Duloxetine on Neuropathic Allodynia-like Signs in Rats. Reviewed International journal

    Tadayuki Ishibashi, Daichi Sueto, Yu Yoshikawa, Keisuke Koga, Ken Yamaura, Makoto Tsuda

    Cells   11 ( 24 )   4051   2022.12   eISSN:20734409

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    Neuropathic pain is a chronic pain condition that occurs after nerve damage; allodynia, which refers to pain caused by generally innocuous stimuli, is a hallmark symptom. Although allodynia is often resistant to analgesics, the antidepressant duloxetine has been used as an effective therapeutic option. Duloxetine increases spinal noradrenaline (NA) levels by inhibiting its transporter at NAergic terminals in the spinal dorsal horn (SDH), which has been proposed to contribute to its pain-relieving effect. However, the mechanism through which duloxetine suppresses neuropathic allodynia remains unclear. Here, we identified an SDH inhibitory interneuron subset (captured by adeno-associated viral (AAV) vectors incorporating a rat neuropeptide Y promoter; AAV-NpyP+ neurons) that is mostly depolarized by NA. Furthermore, this excitatory effect was suppressed by pharmacological blockade or genetic knockdown of α1B-adrenoceptors (ARs) in AAV-NpyP+ SDH neurons. We found that duloxetine suppressed Aβ fiber-mediated allodynia-like behavioral responses after nerve injury and that this effect was not observed in AAV-NpyP+ SDH neuron-selective α1B-AR-knockdown. These results indicate that α1B-AR and AAV-NpyP+ neurons are critical targets for spinal NA and are necessary for the therapeutic effect of duloxetine on neuropathic pain, which can support the development of novel analgesics.

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  • Controlled activation of cortical astrocytes modulates neuropathic pain-like behaviour. Reviewed International journal

    Ikuko Takeda, Kohei Yoshihara, Dennis L Cheung, Tomoko Kobayashi, Masakazu Agetsuma, Makoto Tsuda, Kei Eto, Schuichi Koizumi, Hiroaki Wake, Andrew J Moorhouse, Junichi Nabekura

    Nature communications   13 ( 1 )   4100 - 4100   2022.7

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    Chronic pain is a major public health problem that currently lacks effective treatment options. Here, a method that can modulate chronic pain-like behaviour induced by nerve injury in mice is described. By combining a transient nerve block to inhibit noxious afferent input from injured peripheral nerves, with concurrent activation of astrocytes in the somatosensory cortex (S1) by either low intensity transcranial direct current stimulation (tDCS) or via the chemogenetic DREADD system, we could reverse allodynia-like behaviour previously established by partial sciatic nerve ligation (PSL). Such activation of astrocytes initiated spine plasticity to reduce those synapses formed shortly after PSL. This reversal from allodynia-like behaviour persisted well beyond the active treatment period. Thus, our study demonstrates a robust and potentially translational approach for modulating pain, that capitalizes on the interplay between noxious afferents, sensitized central neuronal circuits, and astrocyte-activation induced synaptic plasticity.

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  • Selective Involvement of a Subset of Spinal Dorsal Horn Neurons Operated by a Prodynorphin Promoter in Aβ Fiber-Mediated Neuropathic Allodynia-Like Behavioral Responses in Rats Reviewed

    Tadayuki Ishibashi, Yu Yoshikawa, Daichi Sueto, Ryoichi Tashima, Hidetoshi Tozaki-Saitoh, Keisuke Koga, Ken Yamaura, Makoto Tsuda

    Frontiers in Molecular Neuroscience   15   911122   2022.6   ISSN:16625099 eISSN:1662-5099

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    Mechanical allodynia (pain produced by innocuous stimuli such as touch) is the main symptom of neuropathic pain. Its underlying mechanism remains to be elucidated, but peripheral nerve injury (PNI)-induced malfunction of neuronal circuits in the central nervous system, including the spinal dorsal horn (SDH), is thought to be involved in touch-pain conversion. Here, we found that intra-SDH injection of adeno-associated viral vectors including a prodynorphin promoter (AAV-PdynP) captured a subset of neurons that were mainly located in the superficial laminae, including lamina I, and exhibited mostly inhibitory characteristics. Using transgenic rats that enable optogenetic stimulation of touch-sensing Aβ fibers, we found that the light-evoked paw withdrawal behavior and aversive responses after PNI were attenuated by selective ablation of AAV-PdynP-captured SDH neurons. Notably, the ablation had no effect on withdrawal behavior from von Frey filaments. Furthermore, Aβ fiber stimulation did not excite AAV-PdynP<sup>+</sup> SDH neurons under normal conditions, but after PNI, this induced excitation, possibly due to enhanced Aβ fiber-evoked excitatory synaptic inputs and elevated resting membrane potentials of these neurons. Moreover, the chemogenetic silencing of AAV-PdynP<sup>+</sup> neurons of PNI rats attenuated the Aβ fiber-evoked paw withdrawal behavior and c-FOS expression in superficial SDH neurons. Our findings suggest that PNI renders AAV-PdynP-captured neurons excitable to Aβ fiber stimulation, which selectively contributes to the conversion of Aβ fiber-mediated touch signal to nociceptive. Thus, reducing the excitability of AAV-PdynP-captured neurons may be a new option for the treatment of neuropathic allodynia.

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  • Chemogenetic silencing of spinal cord-projecting cortical neurons attenuates Aβ fiber-derived neuropathic allodynia in mice. Reviewed International journal

    Kazuki Fujimori, Misuzu Sekine, Moeka Watanabe, Ryoichi Tashima, Hidetoshi Tozaki-Saitoh, Makoto Tsuda

    Neuroscience research   181   115 - 119   2022.5   ISSN:01680102

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    Mechanical allodynia (pain caused by innocuous mechanical stimulation) is a hallmark symptom of neuropathic pain occurring following peripheral nerve injury (PNI). Using a transgenic mouse line, in which myelinated primary afferents, including Aβ fibers, express channelrhodopsin-2, we found that illumination of the plantar skin of mice following PNI produced an Aβ fiber-mediated pain-like withdrawal behavior and increased c-FOS+ neurons in the superficial spinal dorsal horn (SDH). These two responses were attenuated by chemogenetic silencing of primary sensory cortex (S1) neurons projecting directly to the SDH. These findings indicate that spinally projecting cortical S1 neurons contribute to Aβ fiber-derived neuropathic allodynia.

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  • Specification of CNS macrophage subsets occurs postnatally in defined niches. Reviewed International journal

    Takahiro Masuda, Lukas Amann, Gianni Monaco, Roman Sankowski, Ori Staszewski, Martin Krueger, Francesca Del Gaudio, Liqun He, Neil Paterson, Elisa Nent, Francisco Fernández-Klett, Ayato Yamasaki, Maximilian Frosch, Maximilian Fliegauf, Lance Fredrick Pahutan Bosch, Hatice Ulupinar, Nora Hagemeyer, Dietmar Schreiner, Cayce Dorrier, Makoto Tsuda, Claudia Grothe, Anne Joutel, Richard Daneman, Christer Betsholtz, Urban Lendahl, Klaus-Peter Knobeloch, Tim Lämmermann, Josef Priller, Katrin Kierdorf, Marco Prinz

    Nature   604 ( 7907 )   740 - 748   2022.4   ISSN:00280836

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    All tissue-resident macrophages of the central nervous system (CNS)-including parenchymal microglia, as well as CNS-associated macrophages (CAMs1) such as meningeal and perivascular macrophages2-7-are part of the CNS endogenous innate immune system that acts as the first line of defence during infections or trauma2,8-10. It has been suggested that microglia and all subsets of CAMs are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors11-15. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAM subsets in situ are poorly understood. Here we show, using fate-mapping systems, single-cell profiling and cell-specific mutants, that only meningeal macrophages and microglia share a common prenatal progenitor. By contrast, perivascular macrophages originate from perinatal meningeal macrophages only after birth in an integrin-dependent manner. The establishment of perivascular macrophages critically requires the presence of arterial vascular smooth muscle cells. Together, our data reveal a precisely timed process in distinct anatomical niches for the establishment of macrophage subsets in the CNS.

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  • The Function of Glial Cells in the Neuroinflammatory and Neuroimmunological Responses. Reviewed International journal

    Ruqayya Afridi, Makoto Tsuda, Hoon Ryu, Kyoungho Suk

    Cells   11 ( 4 )   2022.2

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    The historical concept of glia just as the glue of brain tissue has been challenged by the accumulation of concrete evidence showing the multifunctional role of these cells during development and in the adult brain [...].

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  • Stress-induced antinociception to noxious heat requires α1A-adrenaline receptors of spinal inhibitory neurons in mice. Reviewed International journal

    Sawako Uchiyama, Kohei Yoshihara, Riku Kawanabe, Izuho Hatada, Keisuke Koga, Makoto Tsuda

    Molecular brain   15 ( 1 )   6 - 6   2022.1

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    It is well known that acute exposure to physical stress produces a transient antinociceptive effect (called stress-induced analgesia [SIA]). One proposed mechanism for SIA involves noradrenaline (NA) in the central nervous system. NA has been reported to activate inhibitory neurons in the spinal dorsal horn (SDH), but its in vivo role in SIA remains unknown. In this study, we found that an antinociceptive effect on noxious heat after acute exposure to restraint stress was impaired in mice with a conditional knockout of α1A-adrenaline receptors (α1A-ARs) in inhibitory neurons (Vgat-Cre;Adra1aflox/flox mice). A similar reduction was also observed in mice treated with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine, a selective neurotoxin for NAergic neurons in the locus coeruleus (LC). Furthermore, whole-cell patch-clamp recordings using spinal cord slices revealed that NA-induced increase in the frequency of spontaneous inhibitory postsynaptic currents in the substantia gelatinosa neurons was suppressed by silodosin, an α1A-AR antagonist, and by conditional knockout of α1A-ARs in inhibitory neurons. Moreover, under unstressed conditions, the antinociceptive effects of intrathecal NA and phenylephrine on noxious heat were lost in Vgat-Cre;Adra1aflox/flox mice. Our findings suggest that activation of α1A-ARs in SDH inhibitory neurons, presumably via LC-NAergic neurons, is necessary for SIA to noxious heat.

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  • Improvement of the affinity of an anti-rat P2X4 receptor antibody by introducing electrostatic interactions. Reviewed International journal

    Chinatsu Shinozaki, Keita Kohno, Mitsunori Shiroishi, Daisuke Takahashi, Yu Yoshikawa, Yoshito Abe, Kenji Hamase, Makoto Nakakido, Kohei Tsumoto, Kazuhide Inoue, Makoto Tsuda, Tadashi Ueda

    Scientific reports   12 ( 1 )   131 - 131   2022.1

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    We have recently developed a mouse monoclonal antibody (12-10H) binding to the head domain region in rat P2X4 receptor (rP2X4R, which is crucial for the pathogenesis of neuropathic pain) expressed on the cell with the highest binding affinity (KD = 20 nM). However, the 12-10H antibody failed to detect endogenously expressed P2X4Rs in microglia isolated from the spinal cord of rats whose spinal nerves were injured. Then, we prepared R5 mutant, in which five arginine residues were introduced into variable regions except for the "hot spot" in the 12-10H antibody to increase electrostatic interactions with the head domain, an anionic region, in rP2X4R. The mutation resulted in an increase of 50-fold in the affinity of the R5 mutant for the head domain with respect to the intact 12-10H antibody. As a result, detection of P2X4Rs endogenously expressed on primary cultured microglial cells originated from the neonatal rat brain and spinal cord microglia isolated from a rat model of neuropathic pain was achieved. These findings suggest a strategy to improve the affinity of a monoclonal antibody for an anionic antigen by the introduction of several arginine residues into variable regions other than the "hot spot" in the paratope.

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  • Role of microglia in reserpine-induced mechanical pain, a model of fibromyalgia

    Saitoh Hidetoshi, Hosoi Masako, Tsuda Makoto

    Proceedings for Annual Meeting of The Japanese Pharmacological Society   95 ( 0 )   2-O-064   2022   eISSN:24354953

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    <p>Chronic widespread pain is a serious problem in our life; fibromyalgia is a well-known disease that causes chronic widespread pain, which might be ascribed to central sensitization. Repeated injection of reserpine, which depletes monoamines in the nervous system, has been used as an animal model of fibromyalgia. Repeated subcutaneous injection of reserpine induces behaviors associated with pain. Microglia in the spinal cord is one of the conceivable factors for the mechanism of central sensitization. However, it is still unclear whether and how microglia in the specific region of the brain affect pain perception.</p><p>Using CX3CR1-CreERT2 mice, we generated microglia-selective knockout mice of IRF8 or MafB, both of which have been previously confirmed to exhibit reduced symptoms of nerve injury-induced neuropathic pain. We found that these mice showed significant suppression of reserpine-induced mechanical hypersensitivity. Since no apparent morphological activation of microglia was seen in the spinal cord and the prefrontal cortex at 5 days after reserpine injection, we performed single-cell RNA sequencing with 10X Genomics Chromium platform on CD11b- and P2Y12-positive cells in the prefrontal and anterior cingulate cortex. Through a non-biased graph-based clustering analysis, we detected populational change among detected clusters. These results support the application of a concept of microglial regulation of reserpine-induced mechanical pain and also suggest functional alteration of prefrontal microglia in the symptom.</p>

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  • Activation of spinal dorsal horn astrocytes by noxious stimuli involves descending noradrenergic signaling. Reviewed International journal

    Riku Kawanabe, Kohei Yoshihara, Izuho Hatada, Makoto Tsuda

    Molecular brain   14 ( 1 )   79 - 79   2021.5

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    Astrocytes are critical regulators of neuronal function in the central nervous system (CNS). We have previously shown that astrocytes in the spinal dorsal horn (SDH) have increased intracellular Ca2+ levels following intraplantar injection of the noxious irritant, formalin. However, the underlying mechanisms remain unknown. We investigated these mechanisms by focusing on the role of descending noradrenergic (NAergic) signaling because our recent study revealed the essential role of the astrocytic Ca2+ responses evoked by intraplantar capsaicin. Using in vivo SDH imaging, we found that the Ca2+ level increase in SDH astrocytes induced by intraplantar formalin injection was suppressed by ablation of SDH-projecting locus coeruleus (LC)-NAergic neurons. Furthermore, the formalin-induced Ca2+ response was dramatically decreased by the loss of α1A-adrenaline receptors (ARs) in astrocytes located in the superficial laminae of the SDH. Moreover, similar inhibition was observed in mice pretreated intrathecally with an α1A-AR-specific antagonist. Therefore, activation of α1A-ARs via descending LC-NAergic signals may be a common mechanism underlying astrocytic Ca2+ responses in the SDH evoked by noxious stimuli, including chemical irritants.

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  • α1A-adrenaline receptors in dorsal horn inhibitory neurons have an inhibitory role in the regulation of chloroquine-induced itch in mice. Reviewed International journal

    Yuto Shiraishi, Keisuke Koga, Ryo Yamagata, Izuho Hatada, Miho Shiratori-Hayashi, Makoto Tsuda

    Molecular brain   14 ( 1 )   55 - 55   2021.3

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    Our previous study showed the intrinsic ability of descending noradrenergic neurons projecting from the locus coeruleus to the spinal dorsal horn (SDH) to suppress itch-related behaviors. Noradrenaline and α1A-adrenaline receptor (α1A-AR) agonist increase inhibitory synaptic inputs onto SDH interneurons expressing gastrin-releasing peptide receptors, which are essential for itch transmission. However, the contribution of α1A-ARs expressed in SDH inhibitory interneurons to itch-related behavior remains to be determined. In this study, RNAscope in situ hybridization revealed that Adra1a mRNA is expressed in SDH inhibitory interneurons that are positive for Slc32a1 mRNA (known as vesicular GABA transporter). Mice with conditional knock-out of α1A-ARs in inhibitory interneurons (Vgat-Cre;Adra1aflox/flox mice) exhibited an increase in scratching behavior when induced by an intradermal injection of chloroquine, but not compound 48/80, which are known as models of histamine-independent and dependent itch, respectively. Furthermore, knockout of inhibitory neuronal α1A-ARs in the SDH using the CRISPR-Cas9 system also increased the scratching behavior elicited by chloroquine but not compound 48/80. Our findings demonstrated for the first time that α1A-ARs in SDH inhibitory interneurons contribute to the regulation of itch signaling with preference for histamine-independent itch.

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  • A Discrete Glycinergic Neuronal Population in the Ventromedial Medulla That Induces Muscle Atonia during REM Sleep and Cataplexy in Mice. Reviewed International journal

    Shuntaro Uchida, Shingo Soya, Yuki C Saito, Arisa Hirano, Keisuke Koga, Makoto Tsuda, Manabu Abe, Kenji Sakimura, Takeshi Sakurai

    The Journal of neuroscience : the official journal of the Society for Neuroscience   41 ( 7 )   1582 - 1596   2021.2

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    During rapid eye movement (REM) sleep, anti-gravity muscle tone and bodily movements are mostly absent, because somatic motoneurons are inhibited by descending inhibitory pathways. Recent studies showed that glycine/GABA neurons in the ventromedial medulla (VMM; GlyVMM neurons) play an important role in generating muscle atonia during REM sleep (REM-atonia). However, how these REM-atonia-inducing neurons interconnect with other neuronal populations has been unknown. In the present study, we first identified a specific subpopulation of GlyVMM neurons that play an important role in induction of REM-atonia by virus vector-mediated tracing in male mice in which glycinergic neurons expressed Cre recombinase. We found these neurons receive direct synaptic input from neurons in several brain stem regions, including glutamatergic neurons in the sublaterodorsal tegmental nucleus (SLD; GluSLD neurons). Silencing this circuit by specifically expressing tetanus toxin light chain (TeTNLC) resulted in REM sleep without atonia. This manipulation also caused a marked decrease in time spent in cataplexy-like episodes (CLEs) when applied to narcoleptic orexin-ataxin-3 mice. We also showed that GlyVMM neurons play an important role in maintenance of sleep. This present study identified a population of glycinergic neurons in the VMM that are commonly involved in REM-atonia and cataplexy.SIGNIFICANCE STATEMENT We identified a population of glycinergic neurons in the ventral medulla that plays an important role in inducing muscle atonia during rapid eye movement (REM) sleep. It sends axonal projections almost exclusively to motoneurons in the spinal cord and brain stem except to those that innervate extraocular muscles, while other glycinergic neurons in the same region also send projections to other regions including monoaminergic nuclei. Furthermore, these neurons receive direct inputs from several brainstem regions including glutamatergic neurons in the sublaterodorsal tegmental nucleus (SLD). Genetic silencing of this pathway resulted in REM sleep without atonia and a decrease of cataplexy when applied to narcoleptic mice. This work identified a neural population involved in generating muscle atonia during REM sleep and cataplexy.

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  • New Inhibitory Effects of Cilnidipine on Microglial P2X7 Receptors and IL-1β Release: An Involvement in its Alleviating Effect on Neuropathic Pain. Reviewed International journal

    Tomohiro Yamashita, Sawako Kamikaseda, Aya Tanaka, Hidetoshi Tozaki-Saitoh, Jose M M Caaveiro, Kazuhide Inoue, Makoto Tsuda

    Cells   10 ( 2 )   2021.2

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    P2X7 receptors (P2X7Rs) belong to a family of ATP-gated non-selective cation channels. Microglia represent a major cell type expressing P2X7Rs. The activation of microglial P2X7Rs causes the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β). This response has been implicated in neuroinflammatory states in the central nervous system and in various diseases, including neuropathic pain. Thus, P2X7R may represent a potential therapeutic target. In the present study, we screened a chemical library of clinically approved drugs (1979 compounds) by high-throughput screening and showed that the Ca2+ channel blocker cilnidipine has an inhibitory effect on rodent and human P2X7R. In primary cultured rat microglial cells, cilnidipine inhibited P2X7R-mediated Ca2+ responses and IL-1β release. Moreover, in a rat model of neuropathic pain, the intrathecal administration of cilnidipine produced a reversal of nerve injury-induced mechanical hypersensitivity, a cardinal symptom of neuropathic pain. These results point to a new inhibitory effect of cilnidipine on microglial P2X7R-mediated inflammatory responses and neuropathic pain, proposing its therapeutic potential.

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  • Reply to Letter to the Editor "Regarding letter on mechanical pain of the lower extremity after compression of the upper spinal cord involves signal transducer and activator of transcription 3-dependent reactive astrocytes and interleukin-6". Reviewed International journal

    Teruaki Ono, Makoto Tsuda

    Brain, behavior, and immunity   91   796 - 796   2021.1

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  • Analysis of binding residues in monoclonal antibody with high affinity for the head domain of the rat P2X4 receptor. Reviewed International journal

    Tatsuhiro Igawa, Shuhei Kishikawa, Yoshito Abe, Makoto Tsuda, Kazuhide Inoue, Tadashi Ueda

    Journal of biochemistry   2020.11

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    P2X4 receptor is known to be involved in neuropathic pain. In order to detect the expression of P2X4 receptor on microglia at the time of onset of neuropathic pain, one approach consist on the preparation of the monoclonal antibodies with both selective binding and high affinity. We have recently established a monoclonal antibody (named 12-10H) which had high affinity to rat P2X4 receptor expressed in 1321N1 cells. The dissociation constants of the complex between the monoclonal antibodies obtained so far and the head domain in the rat P2X4 receptor were in the nanomolar range. To improve the affinity by rational mutations, we need to know the precious location of the binding site in these monoclonal antibodies. Here, we have analyzed and identified the binding residues in the monoclonal antibody (12-10H) with high affinity for the head domain of the rat P2X4 receptor by site-directed mutagenesis.

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  • Role of reactive astrocytes in the spinal dorsal horn under chronic itch conditions. Reviewed

    Miho Shiratori-Hayashi, Makoto Tsuda

    Journal of pharmacological sciences   144 ( 3 )   147 - 150   2020.11

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    Astrocytes are the most abundant glial cells in the central nervous system (CNS), including the spinal cord. Neuronal damage induces astrocytes to become reactive and contribute to various CNS pathologies. Recent studies have demonstrated that astrocytes in the spinal dorsal horn (SDH) become reactive in a transcription factor signal transducer and activator of transcription 3-dependent manner without neuronal damage under chronic itch conditions, causing release of the factor lipocalin-2, leading to induction of sensitization of gastrin releasing peptide-induced chemical itch signaling in the SDH. In this review, we describe recent advances in our understanding of SDH neuronal pathways for itch transmission, the mechanisms of SDH astrocytic activation and its contribution to abnormal itch processing and discuss the role of reactive astrocytes in the SDH in abnormal sensory processing under chronic itch conditions.

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  • Nociceptive signaling mediated by P2X3, P2X4 and P2X7 receptors. Reviewed International journal

    Kazuhide Inoue, Makoto Tsuda

    Biochemical pharmacology   114309 - 114309   2020.10

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    Chronic pain is a debilitating condition that often occurs following peripheral tissue inflammation and nerve injury. This pain, especially neuropathic pain, is a significant clinical problem because of the ineffectiveness of clinically available drugs. Since Burnstock proposed new roles of nucleotides as neurotransmitters, the roles of extracellular ATP and P2 receptors (P2Rs) in pain signaling have been extensively studied, and ATP-P2R signaling has subsequently received much attention as it can provide clues toward elucidating the mechanisms underlying chronic pain and serve as a potential therapeutic target. This review summarizes the literature regarding the role of ATP signaling via P2X3Rs (as well as P2X2/3Rs) in primary afferent neurons and via P2X4Rs and P2X7Rs in spinal cord microglia in chronic pain, and discusses their respective therapeutic potentials.

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  • Intrinsic braking role of descending locus coeruleus noradrenergic neurons in acute and chronic itch in mice. Reviewed International journal

    Keisuke Koga, Yuto Shiraishi, Ryo Yamagata, Hidetoshi Tozaki-Saitoh, Miho Shiratori-Hayashi, Makoto Tsuda

    Molecular brain   13 ( 1 )   144 - 144   2020.10

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    Itch is defined as an unpleasant sensation that provokes a desire to scratch. Our understanding of neuronal circuits for itch information transmission and processing in the spinal dorsal horn (SDH) has progressively advanced following the identification of SDH neuron subsets that are crucial for scratching behavior in models of itch. However, little is known about the control of acute and chronic itch by descending signals from the brain to the SDH. In this study, using genetic approaches that enable cell-type and circuit-specific functional manipulation, we reveal an intrinsic potential of locus coeruleus (LC)-noradrenergic (NAergic) neurons that project to the SDH to control acute and chronic itch. Activation and silencing of SDH-projecting LC-NAergic neurons reduced and enhanced scratching behavior, respectively, in models of histamine-dependent and -independent acute itch. Furthermore, in a model of chronic itch associated with contact dermatitis, repetitive scratching behavior was suppressed by the activation of the descending LC-NAergic pathway and by knocking out NA transporters specific to descending LC-NAergic neurons using a CRISPR-Cas9 system. Moreover, patch-clamp recording using spinal slices showed that noradrenaline facilitated inhibitory synaptic inputs onto gastrin-releasing peptide receptor-expressing SDH neurons, a neuronal subset known to be essential for itch transmission. Our findings suggest that descending LC-NAergic signaling intrinsically controls acute and chronic itch and provide potential therapeutic strategies for the treatment of acute and chronic itch.

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  • Astrocytic phagocytosis is a compensatory mechanism for microglial dysfunction. Reviewed International journal

    Hiroyuki Konishi, Takayuki Okamoto, Yuichiro Hara, Okiru Komine, Hiromi Tamada, Mitsuyo Maeda, Fumika Osako, Masaaki Kobayashi, Akira Nishiyama, Yosky Kataoka, Toshiyuki Takai, Nobuyuki Udagawa, Steffen Jung, Keiko Ozato, Tomohiko Tamura, Makoto Tsuda, Koji Yamanaka, Tomoo Ogi, Katsuaki Sato, Hiroshi Kiyama

    The EMBO journal   e104464   2020.9

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    Microglia are the principal phagocytes that clear cell debris in the central nervous system (CNS). This raises the question, which cells remove cell debris when microglial phagocytic activity is impaired. We addressed this question using Siglechdtr mice, which enable highly specific ablation of microglia. Non-microglial mononuclear phagocytes, such as CNS-associated macrophages and circulating inflammatory monocytes, did not clear microglial debris. Instead, astrocytes were activated, exhibited a pro-inflammatory gene expression profile, and extended their processes to engulf microglial debris. This astrocytic phagocytosis was also observed in Irf8-deficient mice, in which microglia were present but dysfunctional. RNA-seq demonstrated that even in a healthy CNS, astrocytes express TAM phagocytic receptors, which were the main astrocytic phagocytic receptors for cell debris in the above experiments, indicating that astrocytes stand by in case of microglial impairment. This compensatory mechanism may be important for the maintenance or prolongation of a healthy CNS.

    DOI: 10.15252/embj.2020104464

  • The liver-brain-gut neural arc maintains the Treg cell niche in the gut. Reviewed International journal

    Toshiaki Teratani, Yohei Mikami, Nobuhiro Nakamoto, Takahiro Suzuki, Yosuke Harada, Koji Okabayashi, Yuya Hagihara, Nobuhito Taniki, Keita Kohno, Shinsuke Shibata, Kentaro Miyamoto, Harumichi Ishigame, Po-Sung Chu, Tomohisa Sujino, Wataru Suda, Masahira Hattori, Minoru Matsui, Takaharu Okada, Hideyuki Okano, Masayuki Inoue, Toshihiko Yada, Yuko Kitagawa, Akihiko Yoshimura, Mamoru Tanida, Makoto Tsuda, Yusaku Iwasaki, Takanori Kanai

    Nature   585 ( 7826 )   591 - 596   2020.9

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    Recent clinical and experimental evidence has evoked the concept of the gut-brain axis to explain mutual interactions between the central nervous system and gut microbiota that are closely associated with the bidirectional effects of inflammatory bowel disease and central nervous system disorders1-4. Despite recent advances in our understanding of neuroimmune interactions, it remains unclear how the gut and brain communicate to maintain gut immune homeostasis, including in the induction and maintenance of peripheral regulatory T cells (pTreg cells), and what environmental cues prompt the host to protect itself from development of inflammatory bowel diseases. Here we report a liver-brain-gut neural arc that ensures the proper differentiation and maintenance of pTreg cells in the gut. The hepatic vagal sensory afferent nerves are responsible for indirectly sensing the gut microenvironment and relaying the sensory inputs to the nucleus tractus solitarius of the brainstem, and ultimately to the vagal parasympathetic nerves and enteric neurons. Surgical and chemical perturbation of the vagal sensory afferents at the hepatic afferent level reduced the abundance of colonic pTreg cells; this was attributed to decreased aldehyde dehydrogenase (ALDH) expression and retinoic acid synthesis by intestinal antigen-presenting cells. Activation of muscarinic acetylcholine receptors directly induced ALDH gene expression in both human and mouse colonic antigen-presenting cells, whereas genetic ablation of these receptors abolished the stimulation of antigen-presenting cells in vitro. Disruption of left vagal sensory afferents from the liver to the brainstem in mouse models of colitis reduced the colonic pTreg cell pool, resulting in increased susceptibility to colitis. These results demonstrate that the novel vago-vagal liver-brain-gut reflex arc controls the number of pTreg cells and maintains gut homeostasis. Intervention in this autonomic feedback feedforward system could help in the development of therapeutic strategies to treat or prevent immunological disorders of the gut.

    DOI: 10.1038/s41586-020-2425-3

  • Astrocytic STAT3 activation and chronic itch require IP3R1/TRPC-dependent Ca2+ signals in mice. Reviewed International journal

    Miho Shiratori-Hayashi, Chiharu Yamaguchi, Kazushi Eguchi, Yuto Shiraishi, Keita Kohno, Katsuhiko Mikoshiba, Kazuhide Inoue, Motohiro Nishida, Makoto Tsuda

    The Journal of allergy and clinical immunology   2020.8

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    BACKGROUND: Chronic itch is a debilitating symptom of inflammatory skin diseases, but the underlying mechanism is poorly understood. We have recently demonstrated that astrocytes in the spinal dorsal horn become reactive in models of atopic and contact dermatitis via activation of the transcription factor signal transducer and activator of transcription 3 (STAT3) and critically contribute to chronic itch. In general, STAT3 is transiently activated; however, STAT3 activation in reactive astrocytes of chronic itch model mice persistently occurs via an unknown mechanism. OBJECTIVE: We aimed to determine the mechanisms of persistent activation of astrocytic STAT3 in chronic itch conditions. METHODS: To determine the factors that are required for persistent activation of astrocytic STAT3, Western blotting and calcium imaging with cultured astrocytes or spinal cord slices were performed. Thereafter, chronic itch model mice were used for genetic and behavioral experiments to confirm the role of the factors determined to mediate persistent STAT3 activation from in vitro and ex vivo experiments in chronic itch. RESULTS: IP3 receptor type 1 (IP3R1) knockdown in astrocytes suppressed IL-6-induced persistent STAT3 activation and expression of lipocalin-2 (LCN2), an astrocytic STAT3-dependent inflammatory factor that is required for chronic itch. IP3R1-dependent astrocytic Ca2+ responses involved Ca2+ influx through the cation channel transient receptor potential canonical (TRPC), which was required for persistent STAT3 activation evoked by IL-6. IL-6 expression was upregulated in dorsal root ganglion neurons in a mouse model of chronic itch. Dorsal root ganglion neuron-specific IL-6 knockdown, spinal astrocyte-specific IP3R1 knockdown, and pharmacologic spinal TRPC inhibition attenuated LCN2 expression and chronic itch. CONCLUSION: Our findings suggest that IP3R1/TRPC channel-mediated Ca2+ signals elicited by IL-6 in astrocytes are necessary for persistent STAT3 activation, LCN2 expression, and chronic itch, and they may also provide new targets for therapeutic intervention.

    DOI: 10.1016/j.jaci.2020.06.039

  • Physical disuse contributes to widespread chronic mechanical hyperalgesia, tactile allodynia, and cold allodynia through neurogenic inflammation and spino-parabrachio-amygdaloid pathway activation. Reviewed International journal

    Yusuke Ohmichi, Mika Ohmichi, Ryoichi Tashima, Koji Osuka, Kaori Fukushige, Dominika Kanikowska, Yugo Fukazawa, Hiromu Yawo, Makoto Tsuda, Munekazu Naito, Takashi Nakano

    Pain   161 ( 8 )   1808 - 1823   2020.8

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    Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other pathological signs remain unresolved. We have previously reported that inflammatory signs, contractures, disuse muscle atrophy, spontaneous pain-like behaviors, and chronic widespread mechanical hyperalgesia based on central plasticity occurred after 2 weeks of cast immobilization in chronic post-cast pain (CPCP) rat model. In this study, we also demonstrated dystrophy-like changes, both peripheral nociceptive signals and activation of the central pain pathway in CPCP rats. This was done by the following methods: (1) vascular permeability (Evans blue dye) and inflammatory- and oxidative stress-related messenger RNA changes (real-time quantitative polymerase chain reaction); (2) immunofluorescence of pERK and/or c-Fos expression in the spino-parabrachio-amygdaloid pathway; and (3) blockade of nociceptive-related signals using sciatic nerve block. Furthermore, we demonstrated tactile allodynia using an optogenetic method in a transgenic rat line (W-TChR2V4), cold allodynia using the acetone test, and activation of dorsal horn neurons in the chronic phase associated with chronic mechanical hyperalgesia using c-Fos immunofluorescence. In addition, we showed that nociceptive signals in the acute phase are involved in chronic pathological pain-like behaviors by studying the effects of sciatic nerve block. Thus, we conclude that physical disuse contributes to dystrophy-like changes, spontaneous pain-like behavior, and chronic widespread pathological pain-like behaviors in CPCP rats after 2 weeks of cast immobilization.

    DOI: 10.1097/j.pain.0000000000001867

  • Modulation of P2Y6R expression exacerbates pressure overload-induced cardiac remodeling in mice. Reviewed International journal

    Kakeru Shimoda, Akiyuki Nishimura, Caroline Sunggip, Tomoya Ito, Kazuhiro Nishiyama, Yuri Kato, Tomohiro Tanaka, Hidetoshi Tozaki-Saitoh, Makoto Tsuda, Motohiro Nishida

    Scientific reports   10 ( 1 )   13926 - 13926   2020.8

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    Cardiac tissue remodeling caused by hemodynamic overload is a major clinical outcome of heart failure. Uridine-responsive purinergic P2Y6 receptor (P2Y6R) contributes to the progression of cardiovascular remodeling in rodents, but it is not known whether inhibition of P2Y6R prevents or promotes heart failure. We demonstrate that inhibition of P2Y6R promotes pressure overload-induced sudden death and heart failure in mice. In neonatal cardiomyocytes, knockdown of P2Y6R significantly attenuated hypertrophic growth and cell death caused by hypotonic stimulation, indicating the involvement of P2Y6R in mechanical stress-induced myocardial dysfunction. Unexpectedly, compared with wild-type mice, deletion of P2Y6R promoted pressure overload-induced sudden death, as well as cardiac remodeling and dysfunction. Mice with cardiomyocyte-specific overexpression of P2Y6R also exhibited cardiac dysfunction and severe fibrosis. In contrast, P2Y6R deletion had little impact on oxidative stress-mediated cardiac dysfunction induced by doxorubicin treatment. These findings provide overwhelming evidence that systemic inhibition of P2Y6R exacerbates pressure overload-induced heart failure in mice, although P2Y6R in cardiomyocytes contributes to the progression of cardiac fibrosis.

    DOI: 10.1038/s41598-020-70956-5

  • Mechanical pain of the lower extremity after compression of the upper spinal cord involves signal transducer and activator of transcription 3-dependent reactive astrocytes and interleukin-6. Reviewed International journal

    Teruaki Ono, Yuta Kohro, Keita Kohno, Hidetoshi Tozaki-Saitoh, Yasuharu Nakashima, Makoto Tsuda

    Brain, behavior, and immunity   2020.7

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    Chronic pain is one of the main symptoms of spinal disorders such as spinal canal stenosis. A major cause of this pain is related to compression of the spinal cord, and chronic pain can develop at the level of the compressed spinal segment. However, in many patients chronic pain arises in an area that does not correspond to the compressed segment, and the underlying mechanism involved remains unknown. This was investigated in the present study using a mouse model of spinal cord compression in which mechanical pain of the hindpaws develops after compression of the first lumbar segment (L1) of the spinal cord. Compression induced the activation of astrocytes in the L1 spinal dorsal horn (SDH)-but not the L4 SDH that corresponds to the hindpaws-and activated signal transducer and activator of transcription 3 (STAT3). Suppressing reactive astrocytes by expressing a dominant negative form of STAT3 (dnSTAT3) in the compressed SDH prevented mechanical pain. Expression of interleukin (IL)-6 was also upregulated in the compressed SDH, and it was inhibited by astrocytic expression of dnSTAT3. Intrathecal administration of a neutralizing anti-IL-6 antibody reversed the compression-induced mechanical pain. These results suggest that astrocytic STAT3 and IL-6 in the compressed SDH are involved in remote mechanical pain observed in the lower extremity, and may provide a target for treating chronic pain associated with spinal cord compression such as spinal canal stenosis.

    DOI: 10.1016/j.bbi.2020.07.025

  • New pharmacological effect of fulvestrant to prevent oxaliplatin-induced neurodegeneration and mechanical allodynia in rats Reviewed International journal

    Shota Yamamoto, Tomohiro Yamashita, Mayu Ito, Jose M.M. Caaveiro, Nobuaki Egashira, Hidetoshi Tozaki-Saitoh, Makoto Tsuda

    International Journal of Cancer   145 ( 8 )   2107 - 2113   2019.10

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    Oxaliplatin, which is widely used as chemotherapy for certain solid cancers, frequently causes peripheral neuropathy. Commonly described neuropathic symptoms include aberrant sensations such as mechanical allodynia (hypersensitivity to normally innocuous stimuli). Although oxaliplatin neuropathy is a dose-limiting toxicity, there are no established preventive strategies available at present. By screening several sets of small-molecule chemical libraries (more than 3,000 compounds in total) using a newly established in vitro high-throughput phenotypic assay, we identified fulvestrant, a clinically approved drug for the treatment of breast cancer in postmenopausal women, as having a protective effect on oxaliplatin-induced neuronal damage. Furthermore, histological and behavioural analyses using a rat model of oxaliplatin neuropathy demonstrated the in vivo efficacy of fulvestrant to prevent oxaliplatin-induced axonal degeneration of the sciatic nerve and mechanical allodynia. Furthermore, fulvestrant did not interfere with oxaliplatin-induced cytotoxicity against cancer cells. Thus, our findings reveal a previously unrecognised pharmacological effect of fulvestrant to prevent oxaliplatin-induced painful peripheral neuropathy without impairing its cytotoxicity against cancer cells and may represent a novel prophylactic option for patients receiving oxaliplatin chemotherapy.

    DOI: 10.1002/ijc.32043

  • Macrophage centripetal migration drives spontaneous healing process after spinal cord injury Reviewed International journal

    Kazu Kobayakawa, Yasuyuki Ohkawa, Shingo Yoshizaki, Tetsuya Tamaru, Takeyuki Saito, Ken Kijima, Kazuya Yokota, Masamitsu Hara, Kensuke Kubota, Yoshihiro Matsumoto, Katsumi Harimaya, Keiko Ozato, Takahiro Masuda, Makoto Tsuda, Tomohiko Tamura, Kazuhide Inoue, V. Reggie Edgerton, Yukihide Iwamoto, Yasuharu Nakashima, Seiji Okada

    Science Advances   5 ( 5 )   2019.5

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    Traumatic spinal cord injury (SCI) brings numerous inflammatory cells, including macrophages, from the circulating blood to lesions, but pathophysiological impact resulting from spatiotemporal dynamics of macrophages is unknown. Here, we show that macrophages centripetally migrate toward the lesion epicenter after infiltrating into the wide range of spinal cord, depending on the gradient of chemoattractant C5a. However, macrophages lacking interferon regulatory factor 8 (IRF8) cannot migrate toward the epicenter and remain widely scattered in the injured cord with profound axonal loss and little remyelination, resulting in a poor functional outcome after SCI. Time-lapse imaging and P2X/YRs blockade revealed that macrophage migration via IRF8 was caused by purinergic receptors involved in the C5a-directed migration. Conversely, pharmacological promotion of IRF8 activation facilitated macrophage centripetal movement, thereby improving the SCI recovery. Our findings reveal the importance of macrophage centripetal migration via IRF8, providing a novel therapeutic target for central nervous system injury.

    DOI: 10.1126/sciadv.aav5086

  • Transcription factor MafB contributes to the activation of spinal microglia underlying neuropathic pain development Reviewed

    Hidetoshi Saitoh, Junya Masuda, Ryu Kawada, Chinami Kojima, Sosuke Yoneda, Takahiro Masuda, Kazuhide Inoue, Tsuda Makoto

    GLIA   67 ( 4 )   729 - 740   2019.4

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    Microglia, which are pathological effectors and amplifiers in the central nervous system, undergo various forms of activation. A well-studied microglial-induced pathological paradigm, spinal microglial activation following peripheral nerve injury (PNI), is a key event for the development of neuropathic pain but the transcription factors contributing to microglial activation are less understood. Herein, we demonstrate that MafB, a dominant transcriptional regulator of mature microglia, is involved in the pathology of a mouse model of neuropathic pain. PNI caused a rapid and marked increase of MafB expression selectively in spinal microglia but not in neurons. We also found that the microRNA mir-152 in the spinal cord which targets MafB expression decreased after PNI, and intrathecal administration of mir-152 mimic suppressed the development of neuropathic pain. Reduced MafB expression using heterozygous Mafb deficient mice and by intrathecal administration of siRNA alleviated the development of PNI-induced mechanical hypersensitivity. Furthermore, we found that intrathecal transfer of Mafb deficient microglia did not induce mechanical hypersensitivity and that conditional Mafb knockout mice did not develop neuropathic pain after PNI. We propose that MafB is a key mediator of the PNI-induced phenotypic alteration of spinal microglia and neuropathic pain development.

    DOI: 10.1002/glia.23570

  • Hyperactivation of proprioceptors induces microglia-mediated long-lasting pain in a rat model of chronic fatigue syndrome Reviewed

    Masaya Yasui, Yuki Menjyo, Kyohei Tokizane, Akiko Shiozawa, Tsuda Makoto, Kazuhide Inoue, Hiroshi Kiyama

    Journal of Neuroinflammation   16 ( 1 )   2019.3

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    Background: Patients diagnosed with chronic fatigue syndrome (CFS) or fibromyalgia experience chronic pain. Concomitantly, the rat model of CFS exhibits microglial activation in the lumbar spinal cord and pain behavior without peripheral tissue damage and/or inflammation. The present study addressed the mechanism underlying the association between pain and chronic stress using this rat model. Methods: Chronic or continuous stress-loading (CS) model rats, housed in a cage with a thin level of water (1.5 cm in depth), were used. The von Frey test and pressure pain test were employed to measure pain behavior. The neuronal and microglial activations were immunohistochemically demonstrated with antibodies against ATF3 and Iba1. Electromyography was used to evaluate muscle activity. Results: The expression of ATF3, a marker of neuronal hyperactivity or injury, was first observed in the lumbar dorsal root ganglion (DRG) neurons 2 days after CS initiation. More than 50% of ATF3-positive neurons simultaneously expressed the proprioceptor markers TrkC or VGluT1, whereas the co-expression rates for TrkA, TrkB, IB4, and CGRP were lower than 20%. Retrograde labeling using fluorogold showed that ATF3-positive proprioceptive DRG neurons mainly projected to the soleus. Substantial microglial accumulation was observed in the medial part of the dorsal horn on the fifth CS day. Microglial accumulation was observed around a subset of motor neurons in the dorsal part of the ventral horn on the sixth CS day. The motor neurons surrounded by microglia were ATF3-positive and mainly projected to the soleus. Electromyographic activity in the soleus was two to three times higher in the CS group than in the control group. These results suggest that chronic proprioceptor activation induces the sequential activation of neurons along the spinal reflex arc, and the neuronal activation further activates microglia along the arc. Proprioceptor suppression by ankle joint immobilization significantly suppressed the accumulation of microglia in the spinal cord, as well as the pain behavior. Conclusion: Our results indicate that proprioceptor-induced microglial activation may be a key player in the initiation and maintenance of abnormal pain in patients with CFS.

    DOI: 10.1186/s12974-019-1456-x

  • Evidence for detection of rat P2X4 receptor expressed on cells by generating monoclonal antibodies recognizing the native structure Reviewed

    Tatsuhiro Igawa, Shuhei Kishikawa, Yoshito Abe, Tomohiro Yamashita, Saki Nagai, Mitsunori Shiroishi, Chinatsu Shinozaki, Hiroyuki Tanaka, Hidetoshi Saitoh, Tsuda Makoto, Kazuhide Inoue, Tadashi Ueda

    Purinergic Signalling   2019.3

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    P2X purinergic receptors are ATP-driven ionic channels expressed as trimers and showing various functions. A subtype, the P2X4 receptor present on microglial cells is highly involved in neuropathic pain. In this study, in order to prepare antibodies recognizing the native structure of rat P2X4 (rP2X4) receptor, we immunized mice with rP2X4’s head domain (rHD, Gln111–Val167), which possesses an intact structure stabilized by S-S bond formation (Igawa and Abe et al. FEBS Lett. 2015), as an antigen. We generated five monoclonal antibodies with the ability to recognize the native structure of its head domain, stabilized by S-S bond formation. Site-directed mutagenesis revealed that Asn127 and Asp131 of the rHD, in which combination of these amino acid residues is only conserved in P2X4 receptor among P2X family, were closely involved in the interaction between rHD and these antibodies. We also demonstrated the antibodies obtained here could detect rP2X4 receptor expressed in 1321N1 human astrocytoma cells.

    DOI: 10.1007/s11302-019-09646-5

  • Riluzole prevents oxaliplatin-induced cold allodynia via inhibition of overexpression of transient receptor potential melastatin 8 in rats Reviewed

    Shota Yamamoto, Nobuaki Egashira, Tsuda Makoto, Satohiro Masuda

    Journal of Pharmacological Sciences   138 ( 3 )   214 - 217   2018.11

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    Oxaliplatin causes acute cold hypersensitivity in most patients. We previously reported oxalate derived from oxaliplatin induced cold allodynia via overexpression of transient receptor potential melastatin 8 (TRPM8) in the dorsal root ganglion (DRG) in rats. In this study, we examined the effect of riluzole on oxaliplatin-induced cold allodynia. In cultured DRG neurons, riluzole suppressed oxalate-induced increase of the number of menthol (TRPM8 agonist)-sensitive cells. Moreover, riluzole prevented cold allodynia and increase in levels of TRPM8 mRNA in oxaliplatin-treated rats. These results suggest that riluzole prevents oxaliplatin-induced cold allodynia via inhibition of TRPM8 overexpression in the DRG.

    DOI: 10.1016/j.jphs.2018.10.006

  • Interleukin-27 controls basal pain threshold in physiological and pathological conditions Reviewed International journal

    Sasaguri T, Taguchi T, Murata Y, Kobayashi K, Iizasa S, Iizasa E, Tsuda M, Hirakawa N, Hara H, Yoshida H, Yasaka T Interleukin-27 controls basal pain threshold in physiological and pathological conditions.

    Sci Rep   8 ( 1 )   11022   2018.6

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    DOI: 10.1038/s41598-018-29398-3

  • Top-down descending facilitation of spinal sensory excitatory transmission from the anterior cingulate cortex Reviewed

    Tao Chen, Wataru Taniguchi, Qi Yu Chen, Hidetoshi Saitoh, Qian Song, Ren Hao Liu, Kohei Koga, Tsuyoshi Matsuda, Yae Kaito-Sugimura, Jian Wang, Zhi Hua Li, Ya Cheng Lu, Kazuhide Inoue, Tsuda Makoto, Yun Qing Li, Terumasa Nakatsuka, Min Zhuo

    Nature Communications   9 ( 1 )   2018.5

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    Spinal sensory transmission is under descending biphasic modulation, and descending facilitation is believed to contribute to chronic pain. Descending modulation from the brainstem rostral ventromedial medulla (RVM) has been the most studied, whereas little is known about direct corticospinal modulation. Here, we found that stimulation in the anterior cingulate cortex (ACC) potentiated spinal excitatory synaptic transmission and this modulation is independent of the RVM. Peripheral nerve injury enhanced the spinal synaptic transmission and occluded the ACC-spinal cord facilitation. Inhibition of ACC reduced the enhanced spinal synaptic transmission caused by nerve injury. Finally, using optogenetics, we showed that selective activation of ACC-spinal cord projecting neurons caused behavioral pain sensitization, while inhibiting the projection induced analgesic effects. Our results provide strong evidence that ACC stimulation facilitates spinal sensory excitatory transmission by a RVM-independent manner, and that such top-down facilitation may contribute to the process of chronic neuropathic pain.

    DOI: 10.1038/s41467-018-04309-2

  • Temporal Kinetics of Microgliosis in the Spinal Dorsal Horn after Peripheral Nerve Injury in Rodents Reviewed International journal

    Kohno K*, Kitano J*, Kohro Y, Tozaki-Saitoh H, Inoue K, Tsuda M

    Biol Pharm Bull   2018.5

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    DOI: 10.1248/bpb.b18-00278

  • Astrocytic Ca2+ responses in the spinal dorsal horn by noxious stimuli to the skin Reviewed

    Kohei Yoshihara, Tsuyoshi Matsuda, Yuta Koro, Hidetoshi Saitoh, Kazuhide Inoue, Tsuda Makoto

    Journal of Pharmacological Sciences   2018.1

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    The role of astrocytes in the spinal dorsal horn (SDH) for sensory information processing under normal conditions is poorly understood. In this study, we investigated whether SDH astrocytes respond to noxious and innocuous stimuli to the skin of normal mice using in vivo two-photon Ca2+ imaging under anesthesia. We found that noxious stimulation evoked by intraplantar formalin injection provoked an elevation in intracellular Ca2+ levels in SDH astrocytes. By contrast, neither instantaneous noxious pinching nor innocuous stimuli (cooling or brushing) to the hindpaw elicited astrocytic Ca2+ responses. Thus, SDH astrocytes could respond preferentially to a strong and/or sustained noxious stimulus.

    DOI: 10.1016/j.jphs.2018.04.007

  • Specific activation of inhibitory interneurons in the spinal dorsal horn suppresses repetitive scratching in mouse models of chronic itch Reviewed

    Kensho Kanehisa, Miho Shiratori, Keisuke Koga, Hidetoshi Saitoh, Yuta Koro, Kenji Takamori, Tsuda Makoto

    Journal of Dermatological Science   88 ( 2 )   251 - 254   2017.11

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    DOI: 10.1016/j.jdermsci.2017.05.017

  • Fibromyalgia and microglial TNF-α: Translational research using human blood induced microglia-like cells. Reviewed International journal

    Ohgidani M, Kato TA, Hosoi M, Tsuda M, Hayakawa K, Hayaki C, Iwaki R, Sagata N, Hashimoto R, Inoue K, Sudo N, Kanba S

    Sci Rep   7   11882   2017.9

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    DOI: 10.1038/s41598-017-11506-4

  • Chemogenetic silencing of GABAergic dorsal horn interneurons induces morphine-resistant spontaneous nocifensive behaviours. Reviewed International journal

    Koga K, Kanehisa K, Kohro Y, Shiratori-Hayashi M, Tozaki-Saitoh H, Inoue K, Furue H, Tsuda M

    Sci Rep   7   4739   2017.7

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    DOI: 10.1038/s41598-017-04972-3

  • P2Y12 receptors in primary microglia activate nuclear factor of activated T cell signaling to induce C-C chemokine 3 expression Reviewed International journal

    Hidetoshi Saitoh et al.

    J Neurochem   141   100 - 110   2017.4

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  • Cardiac myofibroblast engulfment of dead cells facilitates recovery after myocardial infarction Reviewed International journal

    Nakaya Michio et al.

    J Clin Invest   127   383 - 401   2017.1

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  • Inhibition of G0/G1 Switch 2 Ameliorates Renal Inflammation in Chronic Kidney Disease Reviewed International journal

    Matsunaga Naoya et al.

    EBioMedicine   S2352-3964   30463 - 30467   2016.11

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  • Glucocorticoid regulation of ATP release from spinal astrocytes underlies diurnal exacerbation of neuropathic mechanical allodynia Reviewed International journal

    Koyanagi S et al.

    Nat Commun   7   13102   2016.11

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  • Duloxetine inhibits microglial P2X4 receptor function and alleviates neuropathic pain after peripheral nerve injury Reviewed International journal

    Tomohiro Yamashita et al.

    PLoS One   11   e0165189   2016.10

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  • A novel P2X4 receptor-selective antagonist produces anti-allodynic effect in a mouse model of herpetic pain Reviewed International journal

    Matsumura Y et al.

    Sci Rep   6   32461   2016.8

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  • Purinergic P2Y6 receptors heterodimerize with angiotensin AT1 receptors to promote angiotensin II-induced hypertension Reviewed International journal

    Nishimura et al.

    Sci Signal   9   ra7   2016.1

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  • Transcription factor IRF1 is responsible for IRF8-mediated IL-1β expression in reactive microglia Reviewed International journal

    Takahiro Masuda et al.

    J Pharmacol Sci   128 ( 4 )   216 - 220   2015.8

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  • Solution structure of the rat P2X4 receptor head domain involved in inhibitory metal binding. Reviewed International journal

    Igawa T et al.

    FEBS Lett   589   680 - 686   2015.3

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  • Interferon regulatory factor 8 expressed in microglia contributes to tactile allodynia induced by repeated cold stress in rodents. Reviewed International journal

    Akagi et al.,

    J Pharmacol Sci   121   172 - 176   2014.11

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  • A chronic fatigue syndrome model demonstrates mechanical allodynia and muscular hyperalgesia via spinal microglial activation. Reviewed International journal

    Yasui et al.,

    Glia   62 ( 9 )   1407 - 1417   2014.9

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  • IRF8 is a transcriptional determinant for microglial motility. Reviewed International journal

    Masuda Takahiro et al.

    Purinergic Signal   10 ( 3 )   515 - 521   2014.9

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  • Involvement of the chemokine CCL3 and the purinoceptor P2X7 in the spinal cord in paclitaxel-induced mechanical allodynia. Reviewed International journal

    Ohi-ishi et al.,

    Mol Pain   10   53   2014.8

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  • Chemokine (C-C motif) receptor 5 is an important pathological regulator in the development and maintenance of neuropathic pain. Reviewed International journal

    Matsushita K et al.

    Anesthesiology   120 ( 6 )   1491 - 1503   2014.6

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  • Preparation and characterization of a monoclonal antibody against the refolded and functional extracellular domain of rat P2X4 receptor Reviewed International journal

    Igawa T, Higashi S, yoshito abe, Takatoshi Ohkuri, Hiroyuki Tanaka, satoshi morimoto, 山下 智大, TSUDA MAKOTO, Kazuhide Inoue, Tadashi Ueda

    JOURNAL OF BIOCHEMISTRY   153 ( 3 )   275 - 282   2013.3

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    DOI: 10.1093/jb/mvs143

  • GRK6 deficiency in mice causes autoimmune disease due to impaired apoptotic cell clearance Reviewed International journal

    Nakaya Michio, Tajima M, Kosako H, Nakaya T, Hashimoto A, Watari K, Nishihara H, Ohba M, Komiya S, Tani N, Motohiro Nishida, Taniguchi H, Sato Y, Matsumoto M, TSUDA MAKOTO, Kuroda M, Kazuhide Inoue, Hitoshi Kurose

    NATURE COMMUNICATIONS   4   1532   2013.2

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    DOI: 10.1038/ncomms2540

  • (R)- and (S)-4-Amino-3-(trimethylsilyl)methylbutanoic acids ameliorate neuropathic pain without central nervous system-related side effects Reviewed International journal

    Muratake H, Ito A, Toda T, Suzuki H, Fukasawa H, TSUDA MAKOTO, Kazuhide Inoue, Sugiyama K, Shudo K

    BIOORGANIC & MEDICINAL CHEMISTRY LETTERS   22 ( 24 )   7602 - 7604   2012.12

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    DOI: 10.1016/j.bmcl.2012.10.001

  • Microglial Cathepsin B Contributes to the Initiation of Peripheral Inflammation-Induced Chronic Pain Reviewed International journal

    Sun L, Wu Z, Yoshinori Hayashi, Peters C, TSUDA MAKOTO, Kazuhide Inoue, Hiroshi Nakanishi

    JOURNAL OF NEUROSCIENCE   32 ( 33 )   11330 - 11342   2012.8

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1523/JNEUROSCI.0677-12.2012

  • Involvement of protein kinase D in uridine diphosphate-induced microglial macropinocytosis and phagocytosis. Reviewed International journal

    Uesugi A, Kataoka A, Tozaki-Saitoh H, Koga Y, Tsuda M, Robaye B, Boeynaems JM, Inoue K.

    Glia   60 ( 7 )   2012.7

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  • CCL2 promotes P2X4 receptor trafficking to the cell surface of microglia. Reviewed International journal

    Toyomitsu E, Tsuda M, Yamashita T, Tozaki-Saitoh H, Tanaka Y, Inoue K.

    Purinergic Signal.   8 ( 2 )   2012.6

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  • Involvement of vasodilator-stimulated phosphoprotein in UDP-induced microglial actin aggregation via PKC- and Rho-dependent pathways. Reviewed International journal

    Kataoka A, Koga Y, Uesugi A, Tozaki-Saitoh H, Tsuda M, Inoue K.

    Purinergic Signal.   7 ( 4 )   2011.12

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  • Astrocytic P2Y1 receptor is involved in the regulation of cytokine/chemokine transcription and cerebral damage in a rat model of cerebral ischemia. Reviewed International journal

    Kuboyama K, Harada H, Tozaki-Saitoh H, Tsuda M, Ushijima K, Inoue K

    J Cereb Blood Flow Metab   31 ( 9 )   2011.9

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    DOI: 10.1038/jcbfm.2011.49.

  • Nerve injury-activated microglia engulf myelinated axons in a P2Y12 signaling-dependent manner in the dorsal horn. Reviewed International journal

    Maeda M, Tsuda M, Tozaki-Saitoh H, Inoue K, Kiyama H

    Glia   58 ( 15 )   2010.11

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  • Molecular basis for the dosing time-dependency of anti-allodynic effects of gabapentin in a mouse model of neuropathic pain. Reviewed International journal

    Kusunose N, Koyanagi S, Hamamura K, Matsunaga N, Yoshida M, Uchida T, Tsuda M, Inoue K, Ohdo S

    Mol Pain   6   2010.11

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  • P2X7 receptor activation induces CXCL2 production in microglia through NFAT and PKC/MAPK pathways. Reviewed International journal

    Shiratori M, Tozaki-Saitoh H, Yoshitake M, Tsuda M, Inoue K

    J Neurochem   114 ( 3 )   2010.8

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  • Role of PAF receptor in proinflammatory cytokine expression in the dorsal root ganglion and tactile allodynia in a rodent model of neuropathic pain. Reviewed International journal

    Hasegawa S, Kohro Y, Shiratori M, Ishii S, Shimizu T, Tsuda M, Inoue K

    PLoS ONE 5: e10467 (2010)   2010.5

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  • Activation of cytosolic phospholipase A2 in dorsal root ganglion neurons by Ca2+/calmodulin-dependent protein kinase II after peripheral nerve injury Reviewed International journal

    Hasegawa S, Kohro Y, Tsuda M, Inoue K

    Mol Pain   5   2009.5

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  • Intrathecal delivery of PDGF produces tactile allodynia through its receptors in spinal microglia Reviewed International journal

    Masuda J, Tsuda M, Tozaki-Saitoh H, Inoue K

    Mol Pain   5   2009.5

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  • Direct Observation of ATP-Induced Conformational Changes in Single P2X4 Receptors Reviewed International journal

    Shinozaki Y, Sumitomo K, Tsuda M, Koizumi S, Inoue K, Torimitsu K

    PLoS Biol   7 ( 5 )   2009.5

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  • Antidepressants inhibit P2X4 receptor function: a possible involvement in neuropathic pain relief Reviewed International journal

    Nagata K, Imai T, Yamashita T, Tsuda M, Tozaki-Saitoh H, Inoue K.

    Mol Pain   5   2009.4

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  • Activation of P2X7 receptors induces CCL3 production in microglial cells through transcription factor NFAT. Reviewed International journal

    Kataoka A, Tozaki-Saitoh H, Koga Y, Tsuda M, Inoue K

    J Neurochem 108(1): 115-125 (2009)   2009.1

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  • Activation of dorsal horn microglia contributes to diabetes-induced tactile allodynia via extracellular signal-regulated protein kinase signaling Reviewed International journal

    Tsuda M, Ueno H, Kataoka A, Tozaki-Saitoh H, Inoue K

    Glia 56: 378-386 (2008)   2008.3

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  • Lyn tyrosine kinase is required for P2X4 receptor upregulation and neuropathic pain after peripheral nerve injury Reviewed International journal

    Tsuda M, Tozaki-Saitoh H, Masuda T, Toyomitsu E, Tezuka T, Yamamoto T, Inoue K

    Glia 56: 50-58 (2008)   2008.1

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  • P2X receptors-mediated cytosolic phospholipase A2 activation in primary afferent sensory neurons contributes to neuropathic pain Reviewed International journal

    Tsuda M, Hasegawa S, Inoue K

    J Neurochem 103: 1408-1416 (2007)   2007.11

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  • Reduced pain behaviors and ERK activation in primary sensory neurons by peripheral tissue injury in mice lacking platelet-activating factor receptor Reviewed International journal

    Tsuda M, Ishii S, Masuda T, Hasegawa S, Nakamura K, Nagata K, Yamashita T, Furue H, Tozaki-Saito H, Yoshimura M, Koizumi S, Shimizu T and Inoue K

    J Neurochem 102: 1658–1668 (2007)   2007.9

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  • Long-term potentiation of neuronal excitation by neuron-glia interactions in the rat spinal dorsal horn. Reviewed International journal

    Ikeda H, Tsuda M, Inoue K, Murase K.

    Eur J Neurosci. 2007 Mar;25(5):1297-306.   2007.3

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  • Retinoic acids increase P2X2 receptor expression through the 5'-flanking region of P2rx2 gene in rat phaeochromocytoma PC-12 cells. Reviewed International journal

    Tozaki-Saitoh H, Koizumi S, Sato Y, Tsuda M, Nagao T, Inoue K.

    Mol Pharmacol. 2006 Jul;70(1):319-28.   2006.7

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  • Direct excitation of deep dorsal horn neurones in the rat spinal cord by the activation of postsynaptic P2X receptors. Reviewed International journal

    Shiokawa H, Nakatsuka T, Furue H, Tsuda M, Katafuchi T, Inoue K, Yoshimura M.

    J Physiol. 2006 Jun 15;573(Pt 3):753-63.   2006.6

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  • Possible involvement of increase in spinal fibronectin following peripheral nerve injury in upregulation of microglial P2X4, a key molecule for mechanical allodynia. Reviewed International journal

    Nasu-Tada K, Koizumi S, Tsuda M, Kunifusa E, Inoue K.

    Glia. 2006 May;53(7):769-75.   2006.5

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  • Long-lasting change in brain dynamics induced by methamphetamine: enhancement of protein kinase C-dependent astrocytic response and behavioral sensitization. Reviewed International journal

    Narita M, Miyatake M, Shibasaki M, Tsuda M, Koizumi S, Narita M, Yajima Y, Inoue K, Suzuki T.

    J Neurochem. 2005 Jun;93(6):1383-92.   2005.6

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  • Ca2+ waves in keratinocytes are transmitted to sensory neurons: the involvement of extracellular ATP and P2Y2 receptor activation. Reviewed International journal

    Koizumi S, Fujishita K, Inoue K, Shigemoto-Mogami Y, Tsuda M, Inoue K.

    Biochem J. 2004 Jun 1;380(Pt 2):329-38.   380   329 - 338   2004.6

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    DOI: 10.1042/BJ20031089

  • Signaling of ATP receptors in glia-neuron interaction and pain. Reviewed International journal

    Inoue K, Koizumi S, Tsuda M, Shigemoto-Mogami Y.

    Life Sci. 2003 Dec 5;74(2-3):189-97.   74 ( 2-3 )   189 - 197   2003.12

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    DOI: 10.1016/j.lfs.2003.09.006

  • Dynamic inhibition of excitatory synaptic transmission by astrocyte-derived ATP in hippocampal cultures. Reviewed International journal

    Koizumi S, Fujishita K, Tsuda M, Shigemoto-Mogami Y, Inoue K.

    Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11023-8.   100 ( 19 )   11023 - 11028   2003.9

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    DOI: 10.1073/pnas.1834448100

  • Downregulation of P2X3 receptor-dependent sensory functions in A/J inbred mouse strain. Reviewed International journal

    Tsuda M, Shigemoto-Mogami Y, Ueno S, Koizumi S, Ueda H, Iwanaga T, Inoue K.

    Eur J Neurosci. 2002 May;15(9):1444-50.   15 ( 9 )   1444 - 1450   2002.5

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    DOI: 10.1046/j.1460-9568.2002.01982.x

  • Mechanisms underlying extracellular ATP-evoked interleukin-6 release in mouse microglial cell line, MG-5. Reviewed International journal

    Shigemoto-Mogami Y, Koizumi S, Tsuda M, Ohsawa K, Kohsaka S, Inoue K.

    J Neurochem. 2001 Sep;78(6):1339-49.   78 ( 6 )   1339 - 1349   2001.9

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    DOI: 10.1046/j.1471-4159.2001.00514.x

  • Role of endogenous ATP at the incision area in a rat model of postoperative pain. Reviewed International journal

    Tsuda M, Koizumi S, Inoue K.

    Neuroreport. 2001 Jun 13;12(8):1701-4.   12 ( 8 )   1701 - 1704   2001.6

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    DOI: 10.1097/00001756-200106130-00036

  • Modulation of NMDA- and (+)TAN-67-induced nociception by GABA(B) receptors in the mouse spinal cord. Reviewed International journal

    Yajima Y, Narita M, Tsuda M, Imai S, Kamei J, Nagase H, Suzuki T.

    Life Sci. 2000 Dec 29;68(6):719-25.   2000.12

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  • Effects of the non-competitive NMDA receptor antagonist ketamine on morphine-induced place preference in mice. Reviewed International journal

    Suzuki T, Kato H, Aoki T, Tsuda M, Narita M, Misawa M.

    Life Sci. 2000 Jun 16;67(4):383-9.   2000.6

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  • Evidence for the involvement of spinal endogenous ATP and P2X receptors in nociceptive responses caused by formalin and capsaicin in mice. Reviewed International journal

    Tsuda M, Ueno S, Inoue K.

    Br J Pharmacol. 1999 Dec;128(7):1497-504.   1999.12

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  • In vivo pathway of thermal hyperalgesia by intrathecal administration of alpha,beta-methylene ATP in mouse spinal cord: involvement of the glutamate-NMDA receptor system. Reviewed International journal

    Tsuda M, Ueno S, Inoue K.

    Br J Pharmacol. 1999 May;127(2):449-56.   1999.5

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  • Role of metabotropic glutamate receptors in the hypersusceptibility to pentylenetetrazole-induced seizure during diazepam withdrawal. Reviewed International journal

    Suzuki T, Shimizu N, Tsuda M, Soma M, Misawa M.

    Eur J Pharmacol. 1999 Mar 19;369(2):163-8.   1999.3

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  • Effects of the non-competitive NMDA receptor antagonist ifenprodil on the morphine-induced place preference in mice. Reviewed International journal

    Suzuki T, Kato H, Tsuda M, Suzuki H, Misawa M.

    Life Sci. 1999;64(12):PL151-6.   1999.2

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  • Cell type-specific ATP-activated responses in rat dorsal root ganglion neurons. Reviewed International journal

    Ueno S, Tsuda M, Iwanaga T, Inoue K.

    Br J Pharmacol. 1999 Jan;126(2):429-36.   1999.1

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  • NMDA receptor antagonists potently suppress the spontaneous withdrawal signs induced by discontinuation of long-term diazepam treatment in Fischer 344 rats. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Brain Res. 1998 Apr 20;790(1-2):82-90.   1998.4

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  • Hypersusceptibility to DMCM-induced seizures during diazepam withdrawal in mice: evidence for upregulation of NMDA receptors. Reviewed International journal

    Tsuda M, Shimizu N, Yajima Y, Suzuki T, Misawa M.

    Naunyn Schmiedebergs Arch Pharmacol. 1998 Mar;357(3):309-15.   1998.3

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  • Subsensitivity to mitochondrial diazepam binding inhibitor receptor agonist FGIN-1-27-induced antiseizure effect in diazepam-withdrawn mice. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Life Sci. 1998;62(14):PL213-7.   1998.2

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  • Role of nitric oxide in the hypersusceptibility to pentylenetetrazole-induced seizure in diazepam-withdrawn mice. Reviewed International journal

    Tsuda M, Shimizu N, Yajima Y, Suzuki T, Misawa M.

    Eur J Pharmacol. 1998 Feb 26;344(1):27-30.   1998.2

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  • Region-specific changes in [3H]dizocilpine binding in diazepam-withdrawn rats. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Neurosci Lett. 1998 Jan 9;240(2):113-5.   1998.1

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  • Upregulation of NMDA receptor subunit proteins in the cerebral cortex during diazepam withdrawal. Reviewed International journal

    Tsuda M, Chiba Y, Suzuki T, Misawa M.

    Eur J Pharmacol. 1998 Jan 12;341(2-3):R1-2.   1998.1

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  • Age-related decrease in the antiseizure effect of ifenprodil against pentylenetetrazole in mice. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Brain Res Dev Brain Res. 1997 Dec 19;104(1-2):201-4.   1997.12

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  • Aggravation of DMCM-induced seizure by nitric oxide synthase inhibitors in mice. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Life Sci. 1997;60(23):PL339-43.   1997.5

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  • Antinociceptive effect of buprenorphine in mu1-opioid receptor deficient CXBK mice. Reviewed International journal

    Kamei J, Sodeyama M, Tsuda M, Suzuki T, Nagase H.

    Life Sci. 1997;60(22):PL 333-7.   1997.4

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  • Recovery of decreased seizure threshold for pentylenetetrazole during diazepam withdrawal by NMDA receptor antagonists. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Eur J Pharmacol. 1997 Apr 11;324(1):63-6.   1997.4

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  • Role of the NMDA receptor complex in DMCM-induced seizure in mice. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M.

    Neuroreport. 1997 Feb 10;8(3):603-6.   1997.2

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  • Mecamylamine-precipitated nicotine-withdrawal aversion in rats. Reviewed International journal

    Suzuki T, Ise Y, Tsuda M, Maeda J, Misawa M.

    Eur J Pharmacol. 1996 Oct 31;314(3):281-4.   1996.10

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  • Involvement of the opioid system in the anxiolytic effect of diazepam in mice. Reviewed International journal

    Tsuda M, Suzuki T, Misawa M, Nagase H.

    Eur J Pharmacol. 1996 Jun 20;307(1):7-14.   1996.6

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  • Diazepam pretreatment suppresses morphine withdrawal signs in the mouse. Reviewed International journal

    Suzuki T, Tsuda M, Narita M, Funada M, Mizoguchi H, Misawa M.

    Life Sci. 1996;58(4):349-57.   1995.12

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  • Blockade of morphine-induced place preference by diazepam in mice. Reviewed International journal

    Suzuki T, Tsuda M, Funada M, Misawa M.

    Eur J Pharmacol. 1995 Jul 14;280(3):327-30.   1995.7

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  • Potentiation of physical dependence on diazepam by ondansetron in rats. Reviewed International journal

    Mizoguchi H, Shirayama N, Tsuda M, Yoshiike M, Suzuki T, Misawa M.

    Life Sci. 1994;54(9):PL131-6.   1994.7

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Books

  • 実践行動薬理学:脊髄ミクログリアのATP受容体を介する新しい神経障害性疼痛メカニズム

    津田誠,井上和秀(Role:Edit)

    株式会社金芳堂  2010.3 

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    Language:Japanese   Book type:Scholarly book

  • On the role of ATP-gated P2X receptors in acute, inflammatory and neuropathic pain

    Toulme E, Tsuda M, Khakh BS, Inoue K(Role:Edit)

    CRC Press  2009.11 

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    Language:English   Book type:Scholarly book

  • The nociceptive membrane, Current Topics in Membrane 57, Chapter 9. P2X receptors in sensory neurons.

    M. Tsuda, K. Inoue(Role:Edit)

    Elsevier, pp277-310, (2006)  2006.9 

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    Language:English   Book type:Scholarly book

  • 脊髄反射と脊髄/中枢性感作

    津田誠(Role:Joint author)

    「疼痛医学」教科書制作研究会  2020.3 

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    Language:Japanese   Book type:Scholarly book

  • Microglia in the CNS and neuropathic pain

    Tsuda Makoto

    Springer New York LLC  2018.1 

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    Responsible for pages:77-91   Language:English  

    Neuropathic pain occurring after peripheral nerve injury is not simply a consequence of temporal continuity of acute nociceptive signals, but rather of maladaptive nervous system function. Over the past decades, a body of literature has provided evidence for the necessity and sufficiency of microglia, the tissue-resident macrophages of the central nervous system, for nerve injury-induced alterations in synaptic function. Recent studies have also revealed active roles for microglia in brain regions important for emotion and memory. In this chapter, I highlight recent advances in our understanding of the mechanisms that underlie the role of spinal and brain microglia in neuropathic pain, with a focus on how microglia are activated and alter synaptic function. I also discuss the therapeutic potential of microglia from recent advances in the development of new drugs targeting microglia, which may facilitate translation from the bench to bedside.

    DOI: 10.1007/978-981-13-1756-9_7

  • 神経障害性疼痛のメカニズム解析とそれによる創薬について

    津田誠(Role:Joint author)

    一般社団法人 医薬品医療機器レギュラトリーサイエンス財団  2017.11 

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    Language:Japanese   Book type:Scholarly book

  • 神経障害性疼痛における最新メカニズムと創薬への応用

    津田誠(Role:Joint author)

    技術情報協会  2017.8 

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    Language:Japanese   Book type:Scholarly book

  • グリアと神経障害性痛(痛みのScience&Practice)

    津田 誠(Role:Joint author)

    文光堂  2014.5 

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    Language:Japanese   Book type:Scholarly book

  • Intrathecal infusion of microglia cells.

    Masuda Takahiro et al.(Role:Joint author)

    Springer  2013.9 

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    Language:English   Book type:Scholarly book

  • Lentiviral transduction of cultured microglia.

    Masuda Takahiro et al.(Role:Joint author)

    Springer  2013.9 

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    Language:English   Book type:Scholarly book

  • 神経障害性疼痛

    井上 和秀, 津田 誠(Role:Joint author)

    克誠堂出版  2012.10 

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    Responsible for pages:pp24-32「脊髄・二次ニューロンの可塑的変化と神経障害性疼痛」   Language:Japanese   Book type:Scholarly book

  • 慢性疼痛における薬剤選定と治療薬開発

    津田誠,井上和秀(Role:Joint author)

    技術情報協会  2010.6 

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    Language:Japanese   Book type:Scholarly book

  • Chronic pain and microglia: the role of ATP.

    Inoue K, Tsuda M, Koizumi S.(Role:Joint author)

    Novartis Found Symp. 261, 55-64; discussion 64-67, 149-54 (2004).  2004.5 

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    Language:English   Book type:Scholarly book

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Presentations

  • 脳による新たな痛覚制御機構

    津田誠,川邉陸,内山瑳和子,藤森一樹

    第98回日本薬理学会・第102回日本生理学会・第130回日本解剖学会 合同大会(APPW2025)  2025.3 

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    Event date: 2025.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

  • 青斑核ノルアドレナリン神経-脊髄後角アストロサイト連関による痛覚変調機構

    津田誠

    第46回日本疼痛学会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

  • グリア細胞から痛みの慢性化機序に迫る Invited

    津田誠

    第66回歯科基礎医学会学術大会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  • Functional changes in spinal dorsal horn interneurons crucial for neuropathic pain Invited International conference

    Makoto Tsuda

    The 2024 World Life Science Conference (WLSC2024)   2024.10 

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    Event date: 2024.10

    Language:English   Presentation type:Symposium, workshop panel (public)  

  • Regulation of the chronicity of neuropathic pain by spinal cord microglia Invited International conference

    Makoto Tsuda

    17th Annual Meeting of the Chinese Neuroscience Society (CNS2024)  2024.9 

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    Event date: 2024.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

  • Microglial state transition after nerve injury and chronic pain

    Makoto Tsuda

    2024.7 

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    Event date: 2024.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

  • 皮膚からの起痒信号を伝達する末梢一次求心性神経 Invited

    津田誠

    第123回日本皮膚科学会総会  2024.6 

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    Event date: 2024.6

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  • グリア細胞から見えてきた痛みの慢性化メカニズム Invited

    津田誠

    第67回日本手外科学会学術集会  2024.4 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  • グリア細胞の多様性と慢性疼痛 Invited

    津田誠

    日本薬学会第144年会  2024.3 

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    Event date: 2024.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 脊髄における痒み情報伝達と慢性皮膚炎による変調 Invited

    津田誠

    第101回日本生理学会  2024.3 

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    Event date: 2024.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:北九州   Country:Japan  

  • ミクログリアサブセットから明らかになった新しい慢性疼痛メカニズム Invited

    津田誠

    第129回日本解剖学会総会・全国学術集会  2024.3 

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    Event date: 2024.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:沖縄   Country:Japan  

  • Mechanism for chronic pain revealed by glial cells Invited International conference

    Makoto Tsuda

    39th International Annual Meeting in Pharmaceutical Sciences  2024.3 

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    Event date: 2024.3

    Language:English   Presentation type:Oral presentation (invited, special)  

    Country:Thailand  

  • 脊髄後角での痒み選択的神経回路における新たな構成要素 Invited

    津田誠

    第96回日本生化学会大会  2023.10 

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    Event date: 2023.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 痒み感覚の神経伝達機構と皮膚炎による変化 Invited

    津田誠

    第49回日本神経内分泌学会  2023.10 

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    Event date: 2023.10

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • New mechanism for pain chronicity revealed by microglial subset Invited

    Makoto Tsuda

    THE 50th NAITO CONFERENCE  2023.10 

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    Event date: 2023.10

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  • Control of neuropathic pain development and recovery by spinal glial cells Invited

    津田誠

    第46回日本神経科学大会  2023.8 

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    Event date: 2023.8

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 痛みの慢性化と緩和に関わるグリア細胞 Invited

    津田誠

    日本ペインクリニック学会第57回学術集会  2023.7 

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    Event date: 2023.7

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  • 痛みの慢性化と中枢神経系マクロファージ Invited

    津田誠

    第23回日本抗加齢医学会総会  2023.6 

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    Event date: 2023.6

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • A new mechanism for pain chronicity revealed by microglia subset Invited International conference

    Makoto Tsuda

    JSICR/MMCB 2023 Joint Symposium  2023.5 

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    Event date: 2023.5

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • A new mechanism for pain chronicity revealed by microglia Invited International conference

    Makoto Tsuda

    Cold Spring Harbor Asia-GLIA  2023.4 

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    Event date: 2023.4

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  • 神経障害性の痛みにおける新しい慢性化メカニズム Invited

    津田誠

    日本薬学会第143年会  2023.3 

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    Event date: 2023.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:札幌   Country:Japan  

  • グリア研究から難治性慢性疼痛の理解を目指す Invited International conference

    津田誠

    第62回日本定位・機能神経外科学会  2023.1 

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    Event date: 2023.1

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:山口   Country:Japan  

  • ミクログリアから痛みの慢性化メカニズムを探る Invited

    津田誠

    第13回免疫適塾  2023.1 

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    Event date: 2023.1

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:東京(オンライン)   Country:Japan  

  • 慢性疼痛からの自然回復過程におけるグリア細胞の役割 Invited

    津田誠

    第96回日本薬理学会年会  2022.11 

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    Event date: 2022.11 - 2022.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • グリア細胞から慢性疼痛のメカニズムを紐解く Invited

    津田誠

    第26回日本心療内科学会総会・学術大会  2022.11 

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    Event date: 2022.11

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:福岡   Country:Japan  

  • ニューロン-グリア相互作用から考える慢性疼痛のメカニズム Invited

    津田誠

    第54回関東機能的脳外科カンファレンス  2022.9 

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    Event date: 2022.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:東京(オンライン)   Country:Japan  

  • 痛みの慢性化に関わる脊髄後角細胞 Invited

    津田誠

    第28回日本遺伝子細胞治療学会学術集会  2022.7 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛機序から考えられる新たな治療法の可能性を探る Invited

    津田誠

    第56回日本ペインクリニック学会  2022.7 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • 慢性疼痛の緩解と再発に関わるミクログリアサブセット Invited

    津田誠

    Science Café  2022.6 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京(オンライン)   Country:Japan  

  • 慢性疼痛とグリア細胞 ~新たな方向性~ Invited

    津田誠

    日本麻酔科学会第69回学術集会  2022.6 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸   Country:Japan  

  • 痛覚伝達変調におけるグリア細胞の役割 Invited

    津田誠

    第63回日本神経学会学術大会  2022.5 

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    Event date: 2022.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • 痒みの神経回路と慢性化 Invited

    津田誠

    第8回総合アレルギー講習会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:横浜*ハイブリッド   Country:Japan  

  • 皮膚炎に伴う脊髄後角でのかゆみ感作メカニズム

    津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • ミクログリアサブセットによる新しい疼痛制御 Invited

    津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • 神経-グリア相互連関からわかってきた神経障害性疼痛メカニズム Invited

    津田誠

    第19回日本臨床腫瘍学会学術集会  2022.2 

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    Event date: 2022.2

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:京都*ハイブリッド   Country:Japan  

  • 痛みの慢性化メカニズム:グリア細胞と末梢シグナルから考える Invited

    津田誠

    千里ライフサイエンスセミナーS5  2022.1 

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    Event date: 2022.1

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:大阪*オンライン   Country:Japan  

  • グリア細胞から紐解く慢性疼痛メカニズム Invited

    津田誠

    日本薬学会北陸支部特別講演会  2022.1 

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    Event date: 2022.1

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:金沢*オンライン   Country:Japan  

  • 脊髄におけるかゆみ情報伝達と調節 Invited

    津田誠

    環境医学研究所・順天堂かゆみ研究センター第7回学術シンポジウム  2021.12 

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    Event date: 2021.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • 慢性掻痒における一次求心性神経由来NPTX2の役割

    津田誠,兼久賢章,前嶋翔,坂本浩隆,Paul Worley

    第43回日本疼痛学会  2021.12 

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    Event date: 2021.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:愛知*オンライン   Country:Japan  

  • ミクログリアと慢性疼痛:新しい調節機構 Invited

    津田誠

    第43回日本疼痛学会  2021.12 

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    Event date: 2021.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:愛知*オンライン   Country:Japan  

  • 神経-グリア相互作用による痒みの慢性化機構 Invited

    津田誠

    第30回国際痒みシンポジウム  2021.11 

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    Event date: 2021.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京*オンライン   Country:Japan  

  • 慢性疼痛におけるミクログリアの新しい役割

    津田誠

    第94回日本生化学会  2021.11 

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    Event date: 2021.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜*オンライン   Country:Japan  

  • 脊髄後角アストロサイトを介する新しい痛覚調節メカニズム Invited

    津田誠

    第三回形態解析ワークショップ  2021.9 

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    Event date: 2021.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京*オンライン   Country:Japan  

  • 皮膚からの痛覚神経伝達 Invited

    津田誠

    第29回日本発汗学会  2021.9 

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    Event date: 2021.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:広島*オンライン   Country:Japan  

  • アストロサイトサブセットによる新しい疼痛制御機構 Invited

    津田誠

    生体機能と創薬シンポジウム2020-2021  2021.8 

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    Event date: 2021.8

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:札幌*ハイブリッド   Country:Japan  

  • グリア細胞がつくる新しい痛覚感作機構 Invited

    津田誠

    第14回日本緩和医療薬学会年会  2021.5 

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    Event date: 2021.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:岡山*オンライン   Country:Japan  

  • Role of spinal glial cells in the chronicity of pain Invited

    津田誠

    第98回日本生理学会大会  2021.3 

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    Event date: 2021.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:名古屋 *WEB開催   Country:Japan  

  • 神経障害性疼痛とミクログリア ~過去,現在,そして今後~ Invited

    津田誠

    第42回日本疼痛学会  2020.12 

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    Event date: 2020.12

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 慢性疼痛につながる脊髄内ネットワークの変化 Invited

    津田誠

    第13回日本運動器疼痛学会  2020.11 

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    Event date: 2020.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:オンライン   Country:Japan  

  • ノルアドレナリンによる疼痛制御機構:グリア細胞を介する新しいメカニズム Invited

    津田誠

    第50回日本神経精神薬理学会年会・第42回日本生物学的精神医学会年会・第4回日本精神薬学会総会(NPBPPP2020合同年会)  2020.8 

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    Event date: 2020.8

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:オンライン   Country:Japan  

  • 脊髄後角ミクログリアサブセットと神経障害性疼痛 Invited

    津田誠

    日本薬学会第140年会  2020.3 

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    Event date: 2020.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Japan  

  • 痛覚情報伝達とその修飾機構 Invited

    津田誠

    千里ライフサイエンスセミナーN  2019.11 

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    Event date: 2019.11 - 2019.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Japan  

  • ミクログリアサブセットと慢性疼痛 Invited

    津田誠

    第35回Wakoワークショップ  2019.11 

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    Event date: 2019.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • ミクログリアによる痛みの慢性化メカニズム Invited

    津田誠,齊藤秀俊

    第38回日本認知症学会学術集会  2019.11 

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    Event date: 2019.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • Modulation of mechanosensory behavior by a spinal astrocyte population Invited International conference

    Makoto Tsuda

    第48回内藤コンファレンス  2019.10 

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    Event date: 2019.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:札幌   Country:Japan  

  • Pivotal role of spinal astrocytes in the chronicity of itch Invited International conference

    Makoto Tsuda

    International Brain Research Organization (IBRO) World Congress  2019.9 

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    Event date: 2019.9

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:Daegu   Country:Korea, Republic of  

  • 神経障害性疼痛の脊髄内メカニズム Invited

    津田誠

    日本麻酔科学会九州麻酔科学会第57回大会  2019.9 

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    Event date: 2019.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:福岡   Country:Japan  

  • Modulation of somatosensory information processing by the CNS immune cells microglia Invited

    Makoto Tsuda

    第42回日本神経科学大会,第62回日本神経化学会大会(Neuro2019)  2019.7 

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    Event date: 2019.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:新潟   Country:Japan  

  • 神経障害性疼痛の克服に向けた基礎研究からの挑戦 Invited

    津田誠

    日本ペインクリニック学会53回大会  2019.7 

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    Event date: 2019.7

    Language:Japanese  

    Venue:熊本   Country:Japan  

  • 中枢神経系炎症性ミクログリアと慢性疼痛 Invited

    津田誠

    第40回日本・炎症再生医学会  2019.7 

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    Event date: 2019.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • 脳から脊髄への新しい下行性感覚制御メカニズム Invited

    津田誠

    第41回日本疼痛学会  2019.7 

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    Event date: 2019.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:名古屋   Country:Japan  

  • New approach for investigating neuropathic allodynia by optogenetics in rats Invited International conference

    Makoto Tsuda

    The 7th International Congress on Neuropathic Pain (NeuPSIG 2019)  2019.5 

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    Event date: 2019.5

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:London   Country:United Kingdom  

  • 痒みの慢性化メカニズムをグリア細胞から探る Invited

    津田誠

    日本薬学会第139年会  2019.3 

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    Event date: 2019.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:千葉   Country:Japan  

  • 脊髄後角アストロサイトサブポピュレーションによる体性感覚制御

    津田誠

    第92回日本薬理学会年会  2019.3 

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    Event date: 2019.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Japan  

  • 慢性的な痒みと脊髄グリア細胞 Invited

    津田誠

    生体機能と創薬シンポジウム2018  2018.8 

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    Event date: 2018.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • Modulation of pain processing by spinal cord glia International conference

    Makoto Tsuda

    2018 Toronto Symposium on Synaptic Plasticity in Health and Diseases  2018.8 

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    Event date: 2018.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:Toronto   Country:Japan  

  • 感覚情報処理における脊髄グリア細胞の役割 Invited

    津田誠

    第31回日本顎関節学会・第23回日本口腔顔面痛学会・第33回日本歯科心身医学会 合同大会  2018.7 

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    Event date: 2018.7

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:北九州   Country:Japan  

  • Seeking the mechanisms of chronic itch by scratching: sensory neurons, circuits, and glia Invited International conference

    Makoto Tsuda

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  2018.7 

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    Event date: 2018.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:京都   Country:Japan  

  • 脊髄後角のニューロン・グリア相互作用が作り出す慢性掻痒

    津田誠

    第40回日本疼痛学会  2018.6 

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    Event date: 2018.6

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:長崎   Country:Japan  

  • 慢性掻痒の神経系メカニズム Invited

    津田誠

    第117回日本皮膚科学会総会  2018.6 

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    Event date: 2018.5 - 2018.6

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:広島   Country:Japan  

  • 痒みの神経伝達機構 Invited

    津田誠

    第117回日本皮膚科学会総会  2018.6 

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    Event date: 2018.5 - 2018.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:広島   Country:Japan  

  • 脊髄後角における体性感覚情報処理とグリア細胞 Invited

    津田誠

    第一回三融会主催武田神経科学シンポジウム  2018.3 

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    Event date: 2018.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Microglial modulation of neuropathic pain Invited International conference

    Makoto Tsuda

    Translational Pain Research Symposium  2017.6 

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    Event date: 2018.4

    Language:English   Presentation type:Oral presentation (general)  

    Country:China  

  • グリア細胞から紐解く神経障害性疼痛メカニズム Invited

    津田 誠

    第39回日本疼痛学会  2017.6 

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    Event date: 2018.4

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  • かゆみの慢性化における脊髄後角アストロサイトの関与 Invited

    津田誠

    順天堂大学環境医学研究所 特別学術シンポジウム  2017.6 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • Purinergic stimulation of spinal microglia contributes to chronic pain Invited International conference

    Makoto Tsuda

    XIII European Meeting on Glial Cells in Health and Disease  2017.7 

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    Event date: 2018.4

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:United Kingdom  

  • 脊髄後角アストロサイトによる体性感覚情報プロセシング変化

    津田 誠,高露雄太,井上和秀

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会 合同年会  2017.9 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • Glial cells: key elements for the pathogenesis of neuropathic pain Invited International conference

    Makoto Tsuda

    Asia Dry Eye Summit 2017  2017.10 

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    Event date: 2018.4

    Language:English   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  • Modulation of mechanical sensitivity by spinal glial cells Invited International conference

    Makoto Tsuda

    7th Asian pain symposium  2017.10 

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    Event date: 2018.4

    Language:English   Presentation type:Oral presentation (general)  

    Country:Taiwan, Province of China  

  • 慢性疼痛発症のメカニズムから考える神経障害性疼痛の治療標的 Invited

    津田誠

    第352回福岡臨床整形外科医会研修会  2017.11 

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    Event date: 2018.4

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  • 基礎から痛みを学ぶ Invited

    津田誠

    角膜カンファランス2018  2018.2 

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    Event date: 2018.4

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:広島   Country:Japan  

  • アトピー性皮膚炎等の慢性掻痒に対する中枢神経系を標的にした創薬戦略 Invited

    津田 誠

    日本薬学会第137年会  2017.3 

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    Event date: 2017.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:仙台   Country:Japan  

  • 神経障害性アロディニア研究における光遺伝学を用いた新たな道 Invited

    津田 誠

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:長崎   Country:Japan  

  • 慢性のかゆみの原因を解き明かす Invited

    津田 誠

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

    Venue:長崎   Country:Japan  

  • P2Xチャネルを介したミクログリアの活性化と慢性疼痛 Invited

    津田 誠

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:長崎   Country:Japan  

  • Glial cells in the spinal cord and chronic pain Invited International conference

    TSUDA MAKOTO

    19th Takeda Science Foundation Symposium on Bioscience  2017.1 

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    Event date: 2017.1

    Language:English   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Japan  

  • Glial cells in the spinal dorsal horn: key players for chronic pain and itch Invited

    津田 誠

    第21回グリア研究会  2016.12 

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    Event date: 2016.12

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:大阪   Country:Japan  

  • Microglial purinergic signaling and neuropathic pain Invited International conference

    TSUDA MAKOTO

    46th Annual Meeting Society for Neuroscience  2016.11 

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    Event date: 2016.11

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:San Diego   Country:United States  

  • Spinal microglia activated by purinergic receptors and neuropathic pain Invited International conference

    TSUDA MAKOTO

    PSK-PSJ joint-symposium in 2016  2016.10 

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    Event date: 2016.10

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Seoul   Country:Korea, Republic of  

  • Crucial role of spinal dorsal horn astrocytes in itch chronicity Invited

    津田 誠

    第26回国際痒みシンポジウム  2016.10 

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    Event date: 2016.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • 痛みと痒みの慢性化とグリア細胞 Invited

    津田 誠

    第36回鎮痛薬オピオイドペプチドシンポジウム  2016.8 

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    Event date: 2016.8

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:札幌   Country:Japan  

  • 痛みの慢性化に重要なグリア細胞 Invited

    津田 誠

    第46回日本神経精神薬理学会年会  2016.7 

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    Event date: 2016.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:Seoul   Country:Korea, Republic of  

  • Spinal Microglia Activated by Purinergic Signaling and Neuropathic Pain Invited International conference

    TSUDA MAKOTO

    Keystone Symposia on Microglia in the Brain  2016.6 

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    Event date: 2016.6

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Colorado   Country:United States  

  • 痒みの慢性化と脊髄後角アストロサイト Invited

    津田 誠

    第115回日本皮膚科学会総会  2016.5 

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    Event date: 2016.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Japan  

  • 脊髄後角アストロサイトによる感覚情報伝達変調 Invited

    津田 誠

    第24回日本腰痛学会  2016.4 

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    Event date: 2016.4 - 2017.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:山梨   Country:Japan  

  • 神経障害性疼痛におけるP2X4受容体陽性ミクログリアの役割 Invited

    津田 誠ら

    日本薬学会第136年会  2016.3 

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    Event date: 2016.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 神経障害性疼痛の解明を目指した光遺伝学アプローチ Invited

    津田 誠

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • A crucial role of spinal astrocytes in chronic itch Invited

    津田 誠

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • Microglial purinergic signaling in the spinal cord and neuropathic pain Invited International conference

    津田 誠

    6th Asian Pain Symposium  2015.11 

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    Event date: 2015.11

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Suzhou   Country:China  

  • 難治性疼痛におけるグリア細胞ATP受容体の関与 Invited

    津田 誠

    第9回日本緩和医療薬学会年会  2015.10 

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    Event date: 2015.10

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • Dorsal horn astrocytes: new player in chronic itch Invited International conference

    津田 誠

    8th World Congress on Itch (WCI 2015)  2015.9 

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    Event date: 2015.9

    Language:English   Presentation type:Oral presentation (invited, special)  

    Venue:nara   Country:Japan  

  • 体性感覚系疾患におけるグリア細胞の役割 Invited

    津田 誠

    第45回日本神経精神薬理学会  2015.9 

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    Event date: 2015.9

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • Microglial transcription factors and neuropathic pain Invited

    津田 誠ら

    第58回日本神経化学会大会  2015.9 

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    Event date: 2015.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:さいたま   Country:Japan  

  • Spinal glial cells and chronic pain Invited International conference

    津田 誠ら

    2015 Cold Spring Harbor Asia Conference  2015.6 

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    Event date: 2015.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Suzhou   Country:China  

  • Microglia as a pain maker in neuropathic pain: Rodent studies Invited International conference

    津田 誠

    13th World Congress of Biological Psychiatry  2015.6 

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    Event date: 2015.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Athens   Country:Greece  

  • 脊髄グリア細胞からの研究アプローチ Invited

    津田 誠ら

    第29回日本整形外科学会基礎学術集会  2014.10 

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    Event date: 2014.10

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:鹿児島   Country:Japan  

  • Microglial purinoceptors and chronic pain Invited International conference

    TSUDA MAKOTO et al.

    Purines2014  2014.7 

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    Event date: 2014.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Bonn   Country:Germany  

  • Non-cell-autonomous modulation of neuropathic pain by microglia Invited International conference

    TSUDA MAKOTO et al.

    17th World Congress of Basic and Clinical Pharmacology  2014.7 

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    Event date: 2014.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Capetown   Country:South Africa  

  • グリア細胞から見た神経障害性疼痛メカニズム Invited

    津田 誠

    第55回日本神経学会学術大会  2014.5 

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    Event date: 2014.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛-ミクログリアを中心とした病態メカニズム- Invited

    津田 誠

    第43回日本脊椎脊髄病学会学術集会  2014.4 

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    Event date: 2014.4

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:京都   Country:Japan  

  • 神経障害性疼痛-ミクログリアを中心とした病態メカニズム- Invited

    津田 誠

    第43回日本脊椎脊髄病学会学術集会  2014.4 

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    Event date: 2014.4

    Language:Japanese  

    Venue:京都   Country:Japan  

  • かゆみの慢性化における脊髄内メカニズム

    津田 誠, 井上 和秀

    第87回日本薬理学会年会  2014.3 

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    Event date: 2014.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:仙台   Country:Japan  

  • Purinergic signaling and chronic pain Invited International conference

    TSUDA MAKOTO

    Areces Foundation Symposium  2014.3 

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    Event date: 2014.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Madrid   Country:Spain  

  • ミクログリアでのP2X4受容体発現と神経障害性疼痛におけるIRF転写因子ネットワークの役割

    津田 誠, 増田 隆博, 吉永遼平, 岩本祥佑, 田村智彦, 井上 和秀

    日本薬学会第133回年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • アストロサイト特異的STAT3欠損マウスでは神経損傷後のアストロサイトの活性化と神経障害性疼痛が抑制される

    高露雄太, 津田 誠, 坂口瑛美, 齊藤 秀俊, 岡野栄之, 井上 和秀

    日本薬学会第133回年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 転写因子MafBはミクログリアの活性化過程を調節し神経障害性疼痛に関 与する

    齊藤 秀俊, 津田 誠, 井上 和秀

    日本薬学会第133回年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 転写因子IRF8欠損によるATP誘発ミクログリアケモタキシスの抑制

    西本奈央, 増田 隆博, 冨山大輔, 吉永遼平, 田村智彦, 齊藤 秀俊, 津田 誠, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • アストロサイト特異的STAT3欠損は神経損傷後のアストロサイト活性化および神経障害性疼痛を抑制する

    高露雄太, 津田 誠, 坂口瑛美, 齊藤 秀俊, 岡野栄之, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • CCL21による脊髄ミクログリアのMafB発現誘導

    小嶋ちなみ, 齊藤 秀俊, 津田 誠, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 転写因子MafBは末梢神経損傷後の神経障害性疼痛発症に寄与する

    川田竜, 齊藤 秀俊, 増田 隆博, 津田 誠, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 線維筋痛症モデルマウスで発症するアロディニアにおけるIRF8の役割

    赤木貴紀, 津田 誠, 増田 隆博, 齊藤 秀俊, 田村智彦, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • IRF8-IRF5軸は神経障害性疼痛発現を担うP2X4受容体高発現ミクログリアを誘導する

    増田 隆博, 津田 誠, 吉永遼平, 岩本祥佑, 西山晃, 西本奈央, 齊藤 秀俊, 田村智彦, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • IRF8 is a critical transcription factor required for transforming microglia into a reactive phenotype after nerve injury International conference

    Masuda Takahiro, TSUDA MAKOTO, Ryohei Yoshinaga, Hidetoshi Saitoh, Keiko Ozato, Tomohiko Tamura, Kazuhide Inoue

    42th Annual Meeting Society for Neuroscience  2012.10 

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    Event date: 2012.10

    Language:English  

    Venue:New Orleans   Country:United States  

  • Spinal cord microglia in neuropathic pain signaling Invited International conference

    TSUDA MAKOTO, Masuda Takahiro, Kazuhide Inoue

    11th Biennial Meeting of Asian Pacific Society for Neurochemistry and 55th Meeting of Japanese Society for Neurochemistry  2012.10 

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    Event date: 2012.9 - 2012.10

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Kobe   Country:Japan  

  • IRF5 is required for IRF8-derived microglial activation and contributes to neuropathic pain International conference

    Masuda Takahiro, TSUDA MAKOTO, Ryohei Yoshinaga, Tomohiko Tamura, Kazuhide Inoue

    第55回日本神経化学会大会(APSN/JSN 2012)  2012.9 

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    Event date: 2012.9 - 2012.10

    Language:English  

    Venue:Kobe   Country:Japan  

  • 活性化ミクログリアの転写制御と神経障害性疼痛 Invited

    津田 誠, 井上 和秀

    第35回日本神経科学大会Neuro2012  2012.9 

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    Event date: 2012.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:名古屋   Country:Japan  

  • Neuropathic pain:新たな病態解明と画期的新薬の開発をめざして Invited

    津田 誠, 井上 和秀

    第23回日本末梢神経学会学術集会  2012.9 

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    Event date: 2012.8 - 2012.9

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • IRFファミリー転写因子群によるミクログリア遺伝子の発現制御と神経障害性疼痛

    増田 隆博, 津田 誠, 田村智彦, 井上 和秀

    第34回日本疼痛学会  2012.7 

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    Event date: 2012.7

    Language:Japanese  

    Venue:熊本   Country:Japan  

  • IRF8 is a critical transcription for transforming microglia into a reactive phenotype International conference

    TSUDA MAKOTO, Masuda Takahiro, Ryohei Yoshinaga, Hidetoshi Saitoh, Keiko Ozato, Tomohiko Tamura, Kazuhide Inoue

    The 7th International Conference of Neurons and Brain Diseases  2012.6 

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    Event date: 2012.6

    Language:English  

    Venue:Montreal   Country:Canada  

  • IRF Family Transcription Factor Axis Governs Gene Expression Program in Microglia Gating Neuropathic Pain International conference

    Masuda Takahiro, TSUDA MAKOTO, Ryohei Yoshinaga, Nao Nishimoto, Shosuke Iwamoto, Hidetoshi Saitoh, Tomohiko Tamura, Kazuhide Inoue

    Purine 2012  2012.6 

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    Event date: 2012.5 - 2012.6

    Language:English  

    Venue:Fukuoka   Country:Japan  

  • CCL2 promotes P2X4 receptor trafficking to the cell surface of microglia Invited International conference

    Hidetoshi Saitoh, Emika Toyomitsu, TSUDA MAKOTO, 山下 智大, Yoshitaka Tanaka, Kazuhide Inoue

    Purine 2012  2012.5 

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    Event date: 2012.5 - 2012.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Fukuoka   Country:Japan  

  • Transcriptional regulation of P2X4R and neuropathic pain Invited International conference

    TSUDA MAKOTO, Masuda Takahiro, Hidetoshi Saitoh, Kazuhide Inoue

    Purine 2012  2012.5 

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    Event date: 2012.5 - 2012.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Fukuoka   Country:Japan  

  • 難治性慢性疼痛におけるミクログリアの重要性 Invited

    津田誠,井上和秀

    第117回日本解剖学会総会・全国学術集会  2012.3 

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    Event date: 2012.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:山梨県甲府   Country:Japan  

  • 神経障害性疼痛時におけるIRFファミリー転写因子を基軸としたミクログリア遺伝子の発現制御

    増田隆博,津田誠,吉永遼平,西本奈央,岩本祥祐,田村智彦,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Venue:京都市   Country:Japan  

  • グリア細胞の役割から慢性疼痛メカニズムを探る Invited

    津田誠,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:京都市   Country:Japan  

  • 脊髄ミクログリアのinterferon regulatory factor-5は神経障害性疼痛の発現に重要な転写因子である

    吉永遼平,津田誠,増田隆博,西本奈央,齊藤秀俊,田村智彦,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Venue:京都市   Country:Japan  

  • IRF8 is a critical transcription factor required for microglia activation Invited

    Makoto Tsuda, Takahiro Masuda, Kazuhide Inoue

    第34回分子生物学会  2011.12 

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    Event date: 2011.12

    Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 神経障害性疼痛の維持におけるJAK-STAT3 シグナリングの役割

    津田誠,高露雄太,辻川智子,矢野貴之,北野順子,齊藤秀俊,井上和秀

    第39回薬物活性シンポジウム  2011.11 

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    Event date: 2011.11

    Venue:福岡県福岡市   Country:Japan  

  • 神経障害性疼痛に重要なミクログリア転写因子 Invited

    津田誠,増田隆博,齊藤秀俊,井上和秀

    第39回薬物活性シンポジウム  2011.11 

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    Event date: 2011.11

    Presentation type:Symposium, workshop panel (public)  

    Venue:福岡県福岡市   Country:Japan  

  • 神経障害性疼痛とグリア細胞~その役割と分子メカニズム~ Invited

    津田誠,井上和秀

    第4回日本運動器疼痛学会  2011.11 

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    Event date: 2011.11

    Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Japan  

  • Interferon regulatory factor-8は、神経損傷後に見られる脊髄ミクログリアの過活動状態への移行に重要な転写因子である

    増田隆博,津田誠,吉永遼平,齊藤秀俊,田村智彦,井上和秀

    第54回日本神経化学会大会  2011.9 

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    Event date: 2011.9

    Venue:石川県山代温泉   Country:Japan  

  • 脊髄ミクログリアのinterferon regulatory factor-5は神経障害性疼痛の発現に重要な転写因子である

    吉永遼平,津田誠,増田隆博,西本奈央,齋藤秀俊,田村智彦,井上和秀

    第54回日本神経化学会大会  2011.9 

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    Event date: 2011.9

    Venue:石川県山代温泉   Country:Japan  

  • IRF8 transcription factor directs microglia to be a hyperactive phenotype International conference

    Masuda, T.; Tsuda, M.; Yoshinaga, R.; Tozaki-Saitoh, H.; Tamura, T.; Inoue, K.

    10th Euroglia Meeting on Glial Cells in Health and Diseases  2011.9 

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    Event date: 2011.9

    Venue:Prague   Country:Czech Republic  

  • Microglia in pain signaling Invited International conference

    Makoto Tsuda, Takahiro Masuda, Kazuhide Inoue

    10th Euroglia Meeting on Glial Cells in Health and Diseases  2011.9 

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    Event date: 2011.9

    Presentation type:Symposium, workshop panel (public)  

    Venue:Prague   Country:Japan  

  • 脊髄グリア細胞から探る神経障害性疼痛メカニズム Invited

    津田誠,井上和秀

    第16回日本緩和医療学会学術大会  2011.7 

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    Event date: 2011.7

    Presentation type:Symposium, workshop panel (public)  

    Venue:札幌   Country:Japan  

  • Spinal microglia: crucial non-neuronal cells for neuropathic pain Invited International conference

    Makoto Tsuda

    2nd KPRC Seoul Pain Symposium Program  2011.6 

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    Event date: 2011.6

    Presentation type:Symposium, workshop panel (public)  

    Venue:Seoul   Country:Korea, Republic of  

  • 痛みの慢性化を抑制するグリア細胞制御 Invited

    津田誠,井上和秀

    日本麻酔科学会第58回学術集会  2011.5 

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    Event date: 2011.5

    Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • ミクログリアでのP2X4受容体発現を増加させ神経障害性疼痛の形成に関与する損傷ニューロン由来因子CCL21

    津田誠,Knut Biber,齊藤秀俊,塚本恵子,豊満笑加,増田隆博,Hendrikus Boddeke,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • JAK-STAT3シグナリングは神経障害性疼痛の維持に重要な脊髄アストロサイトの増殖を調節する

    津田誠,高露雄太,辻川智子,矢野貴之,北野順子,齊藤秀俊,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • 脊髄ミクログリア細胞-神経因性疼痛の新しい治療薬開発ターゲットになり得るか? Invited

    津田誠,井上和秀

    第25回日本整形外科学会基礎学術集会  2010.10 

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    Event date: 2010.10

    Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Japan  

  • ATP受容体とミクログリア細胞を標的にした新しい鎮痛薬の可能性 Invited

    津田誠,井上和秀

    第4回日本緩和医療薬学会年会  2010.9 

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    Event date: 2010.9

    Presentation type:Symposium, workshop panel (public)  

    Venue:鹿児島   Country:Japan  

  • 脊髄ミクログリア:難治性慢性疼痛における重要な役者 Invited

    津田誠,増田隆博,齊藤秀俊,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • ATP受容体から難治性慢性疼痛メカニズムを探る Invited

    津田誠,井上和秀

    日本薬学会第130年会  2010.3 

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    Event date: 2010.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:岡山   Country:Japan  

  • グリア細胞を標的にした新しい鎮痛薬の可能性 Invited

    津田誠,井上和秀

    日本薬学会第130年会  2010.3 

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    Event date: 2010.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:岡山   Country:Japan  

  • 痛みの慢性化メカニズムにおけるP2Xイオンチャネルの役割 Invited

    津田誠,井上和秀

    日本薬学会第130年会  2010.3 

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    Event date: 2010.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:岡山   Country:Japan  

  • (Medical/Neuroscience) Glia & Diseases: Spinal microglia are key players for understanding mechanisms of intractable chronic pain Invited International conference

    Makoto Tsuda

    4th Symposium of Japanese-French Frontiers of Science (JFFoS)  2010.1 

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    Event date: 2010.1

    Presentation type:Oral presentation (general)  

    Venue:Futuroscope   Country:France  

  • Behavioral phenotypes of mice lacking purinergic P2X4 receptors in acute and chronic pain assays International conference

    Makoto Tsuda, Kazuya Kuboyama, Tomoyuki Inoue, Kenichiro Nagata, Hidetoshi Tozaki-Saitoh and Kazuhide Inoue

    39th Annual Meeting Society for Neuroscience  2009.10 

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    Event date: 2009.10

    Venue:Chicago   Country:United States  

  • ミクログリアと疼痛 Invited

    津田誠,井上和秀

    第52回日本神経化学会大会  2009.6 

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    Event date: 2009.6

    Presentation type:Symposium, workshop panel (public)  

    Venue:群馬・渋川   Country:Japan  

  • 難治性疼痛メカニズム解明への鍵となるミクログリア細胞 Invited

    津田誠,井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 脊髄グリア細胞の役割から慢性痛のメカニズムを探る Invited

    津田誠,井上和秀

    第38回日本慢性疼痛学会  2009.2 

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    Event date: 2009.2

    Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • 慢性疼痛モデルで発現変動する分子の疼痛行動や細胞機能における役割の解析 Invited

    津田誠,井上和秀

    福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • Regulation of neuropathic pain through activated microglia in the spinal cord Invited International conference

    Makoto Tsuda, Takahiro Masuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • World First Discovery and Research-Neuropathic Pain, Neuralgia Invited

    TSUDA MAKOTO

    12th Asia Pacific Pharmaceutical Symposium  2013.8 

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    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:千葉   Country:Japan  

  • 神経障害性疼痛と脊髄グリア細胞 Invited

    津田 誠, 井上 和秀

    日本ペインクリニック学会第47回大会  2013.7 

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    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:大宮   Country:Japan  

  • ミクログリアに発現するATP受容体と神経因性疼痛 Invited

    津田誠,齊藤秀俊,井上和秀

    第81回日本薬理学会年会  2008.3 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Role of spinal microglia in the pathogenesis of neuropathic pain

    津田 誠,井上和秀

    第48回日本神経化学会大会  2005.8 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • P2X4受容体発現制御因子と難治性疼痛

    津田誠,井上和秀

    第79回日本薬理学会年会  2006.3 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 神経およびグリア細胞培養系を利用した疼痛基礎研究

    津田誠

    第112回日本ペインクリニック学会  2006.7 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 慢性疼痛における脊髄グリア細胞の重要性 Invited

    津田誠,井上和秀

    第36回日本慢性疼痛学会  2007.2 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • ATP受容体を介した難治性疼痛発症維持機構

    津田誠

    第80回日本薬理学会年会  2007.3 

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    Country:Japan  

  • ミクログリアのグリア伝達物質と神経因性疼痛 Invited

    津田誠,井上和秀

    第84回日本生理学会大会  2007.3 

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    Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Mechanisms underlying neuropathic pain through spinal microglia Invited

    津田誠

    第50回日本神経化学会大会 / Neuro2007  2007.9 

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    Presentation type:Oral presentation (general)  

    Country:Japan  

  • Src-family tyrosine kinase Lyn in microglia contributes to neuropathic pain after peripheral nerve injury International conference

    Tsuda M, Masuda T, Tezuka T, Kitano J, Yamamoto T, Inoue K

    37th Annual Meeting Society for Neuroscience  2007.11 

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    Venue:San Diego   Country:United States  

  • Role of microglial ATP receptors in neuropathic pain Invited International conference

    Tsuda M, Inoue K

    US-Japan joint meeting for glia research  2008.3 

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    Presentation type:Symposium, workshop panel (public)  

    Venue:Philadelphia   Country:United States  

  • 脳による新たな疼痛発生メカニズム

    津田誠

    日本薬学会第145年会  2025.3 

  • インターロイキン4は脊髄CD11c陽性ミクログリアを増加させることで神経障害性疼痛を緩和する

    河野敬太,白坂亮二,芝田悠人,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 薬学系研究室を主宰する立場で考えるダイバーシティ

    津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

  • 一次体性感覚野から脊髄後角へ直接投射する神経のアロディニアへの関与

    井絵理子,篠塚翔,末藤大智,藤森一樹,山浦健,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 自発痛を誘発する脳-脊髄後角神経路の解析

    角田昂大,藤森一樹,栗野陽平,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Poster presentation  

  • ストレス誘発性痛覚過敏には脊髄後角アストロサイトによるシナプス伝達変調が関与する

    鍵山一輝,内山瑳和子,川邉陸,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  • MRGPRC11活性化物質の探索とそれらの掻痒行動への影響

    山下智大,有松薫乃,田中宏昌,則松綾水,武田眞保,矢崎亮,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Poster presentation  

  • 痛みの生成および過敏化を担う新たな神経サブセットの同定

    藤森一樹,齊藤秀俊,角田昂大,栗野陽平,勢力薫,橋本均,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 正常発達過程およびアルツハイマー病モデルマウスの脳と脊髄におけるCD11c陽性ミクログリアサブセットの時空間的動態

    野巻昂平,藤川理沙子,増田隆博,西道隆臣,齊藤貴志,津田誠

    日本薬学会第145年会  2025.3 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Poster presentation  

  • 活性化アストロサイトは神経障害性アロディニアに重要な脊髄後角抑制性神経の機能低下を誘導する

    末藤大智,石橋忠幸,吉川優,山浦健,津田誠

    第98回日本薬理学会・第102回日本生理学会・第130回日本解剖学会 合同大会(APPW2025)  2025.3 

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    Event date: 2025.3

    Language:English   Presentation type:Oral presentation (general)  

  • 痛みの生成および過敏化させる新たな神経サブセットの同定

    藤森一樹,齊藤秀俊,角田昂大,栗野陽平,勢力薫,橋本均,津田誠

    第98回日本薬理学会・第102回日本生理学会・第130回日本解剖学会 合同大会(APPW2025)  2025.3 

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    Event date: 2025.3

    Language:English   Presentation type:Oral presentation (general)  

  • 正常発達過程およびアルツハイマー病モデルマウスにおけるCD11c陽性ミクログリアの時空間解析

    野巻昂平,藤川理沙子,増田隆博,西道隆臣,齊藤貴志,津田誠

    第98回日本薬理学会・第102回日本生理学会・第130回日本解剖学会 合同大会(APPW2025)  2025.3 

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    Event date: 2025.3

    Language:English   Presentation type:Poster presentation  

  • Regulation of pain chronicity by neuro-immune crosstalk Invited

    津田誠

    第53回日本免疫学会学術集会  2024.12 

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    Event date: 2024.12

    Language:English   Presentation type:Symposium, workshop panel (public)  

  • 神経障害性疼痛モデルにおいてミエリン化一次求心性神経の損傷が脊髄ミクログリアの活性化を引き起こす

    芝田悠人,松本祐季,河野敬太,津田誠

    第41回日本薬学会九州山口支部大会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 神経障害性アロディニアに直結する脊髄後角抑制性神経の活動低下には活性化アストロサイトが必要である

    末藤大智,石橋忠幸,吉川優,山浦健,津田誠

    第46回日本疼痛学会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 疼痛とミクログリアの研究3.0 Invited

    津田誠

    第46回日本疼痛学会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

  • 脊髄のCD11c陽性ミクログリアを増加させることで神経障害性疼痛を緩和に導く

    河野敬太,白坂亮二,津田誠

    第46回日本疼痛学会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 有髄神経線維の傷害が脊髄ミクログリアの活性化を誘導する

    松本祐季,芝田悠人,河野敬太,津田誠 

    第46回日本疼痛学会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • マウス脊髄灰白質アストロサイトの高効率および高純度単離法の確立

    高露雄太,岩﨑令真,津田誠

    第77回日本薬理学会西南部会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 脊髄後角アストロサイトによる痛覚伝達変調:ストレス性痛覚過敏への関与

    鍵山一輝,内山瑳和子,川邉陸,津田誠

    第77回日本薬理学会西南部会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 神経障害性疼痛モデルにおける脊髄ミクログリアの活性化には有髄性一次求心性神経の損傷が関与する

    芝田悠人,松本祐季,河野敬太,津田誠

    第77回日本薬理学会西南部会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 発達期から成体期におけるCD11c陽性ミクログリアの時空間解析

    野巻 昂平,藤川 理沙子,増田 隆博,津田 誠

    第23回次世代を担う若手のためのファーマ・バイオフォーラム2024  2024.9 

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    Event date: 2024.9

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 脊髄後角アストロサイトによるシナプス伝達の変調

    鍵山一輝,内山瑳和子,津田誠

    第23回次世代を担う若手のためのファーマ・バイオフォーラム2024  2024.9 

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    Event date: 2024.9

    Language:Japanese   Presentation type:Oral presentation (general)  

  • Mouse line-dependent cellular responses in microglia-targeting genetic tools

    Ayato Yamasaki, Makoto Tsuda, Takahiro Masuda

    NEURO2024(第47回日本神経科学大会・第67回日本神経化学会大会・第46回日本生物学的精神医学会年会)  2024.7 

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    Event date: 2024.7 - 2027.7

    Language:English   Presentation type:Oral presentation (general)  

  • Spinal dorsal horn Hes5+ astrocytes are necessary for stress-induced hyperalgesia

    Riku Kawanabe, Sawako Uchiyama, Makoto Tsuda

    NEURO2024(第47回日本神経科学大会・第67回日本神経化学会大会・第46回日本生物学的精神医学会年会)  2024.7 

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    Event date: 2024.7

    Language:English   Presentation type:Oral presentation (general)  

  • Interleukin-4 alleviates neuropathic pain by increasing CD11c+ microglia

    Keita Kohno, Ryoji Shirasaka, Yuuto Shibata, Makoto Tsuda

    NEURO2024(第47回日本神経科学大会・第67回日本神経化学会大会・第46回日本生物学的精神医学会年会)  2024.7 

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    Event date: 2024.7

    Language:English   Presentation type:Oral presentation (general)  

  • A new method for isolating astrocytes in the gray matter of spinal cord from adult mice

    Yuta Kohro, Ryoma Iwasaki, Makoto Tsuda

    NEURO2024(第47回日本神経科学大会・第67回日本神経化学会大会・第46回日本生物学的精神医学会年会)  2024.7 

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    Event date: 2024.7

    Language:English   Presentation type:Poster presentation  

  • かゆみを感じる仕組み Invited

    津田誠

    日本毒性学会第21回市民公開セミナー  2024.7 

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    Event date: 2024.7

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

  • ミクログリアから見た神経損傷による痛みの慢性化機序 Invited

    津田誠

    第51回日本毒性学会学術年会  2024.7 

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    Event date: 2024.7

  • Bidirectional modulation of somatosensory behavior by noradrenergic signaling through a spinal astrocyte population and inhibitory neurons

    Yuta Kohro, Tsuyoshi Matsuda, Kohei Yoshihara, Riku Kawanabe, Sawako Uchiyama, Makoto Tsuda

    THE 50th NAITO CONFERENCE  2023.10 

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    Event date: 2024.4

    Language:English  

    Country:Japan  

  • アストロサイト-神経相互作用を介した下行性疼痛制御機構の解明 Invited

    高露雄太,松田烈士,吉原康平,川邉陸,内山瑳和子,津田誠

    第45回日本疼痛学会  2023.12 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福島   Country:Japan  

  • 神経障害に伴う慢性疼痛の発症・維持機構 Invited

    津田誠

    第66回日本脳循環代謝学会学術集会  2023.11 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • カンナビノイド受容体1遺伝子プロモーター活性を有する脊髄後角神経サブセットの神経障害性疼痛における役割

    井絵理子、大西晃央、末藤大智、津田誠

    日本薬学会第144年会  2024.3 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • ACSA2抗体と低温活性プロテアーゼを用いた新たな脊髄アストロサイト高純度単離法の確立

    岩﨑令真、高露雄太、津田誠

    日本薬学会第144年会  2024.3 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • CD11c陽性ミクログリアの増加は神経障害性疼痛の緩和を促進する

    河野敬太,白坂亮二,廣瀬恵太,芝田悠人,津田誠

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • Proper distribution and proliferation of microglia involves mechanosensitive channel Piezo1

    Ayato Yamasaki, Makoto Tsuda, Takahiro Masuda

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 脳-脊髄トップダウンシグナルが神経障害性アロディニアに及ぼす影響の網羅的解析

    藤森一樹,齊藤秀俊,勢力薫,橋本均,津田誠

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 神経障害性アロディニアに必要な脊髄後角抑制性神経の機能低下におけるアストロサイトの役割

    末藤大智,石橋忠幸,吉川優,山浦健,津田誠

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • アルツハイマー病モデルマウスの脳内でのCD11c陽性ミクログリアの時空間解析

    野巻昂平,藤川理沙子,増田隆博,西道隆臣,齊藤貴志,津田誠

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • Model of recurrent neuropathic pain by social defeat stress with underlying inflammatory responses

    Hidetoshi Tozaki-Saitoh, Takuya Hatta, Kazuhide Inoue, Makoto Tsuda

    第97回日本薬理学会年会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • Aβ線維由来神経障害性アロディニアに重要な脊髄後角神経回路

    末藤大智,石橋忠幸,吉川優,田島諒一,山浦健,津田誠

    第45回日本疼痛学会  2023.12 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 神経損傷による慢性疼痛に重要な脊髄後角興奮性神経の同定

    大西晃央,末藤大智,井絵理子,津田誠

    第40回日本薬学会九州山口支部大会  2023.11 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • CD11c陽性ミクログリア由来IGF1の疼痛症状寛解作用機序の解析

    廣瀬恵大,河野敬太,津田誠

    第40回日本薬学会九州山口支部大会  2023.11 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 神経障害性疼痛を緩和に導く脊髄ミクログリア

    河野敬太,白坂亮二,廣瀬恵大,芝田悠人,津田誠

    第76回日本薬理学会西南部会  2023.10 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • Aβ神経線維を介する神経障害性アロディニアに重要な脊髄後角興奮性介在神経

    井絵理子,大西晃央,末藤大智,津田誠

    第76回日本薬理学会西南部会  2023.10 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 発達期から成体期におけるCD11c陽性ミクログリアの時空間解析

    野巻昂平,藤川理沙子,増田隆博,津田誠

    第76回日本薬理学会西南部会  2023.10 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 神経障害性アロディニアの発症に関与する脊髄後角興奮性神経

    井絵理子,大西晃央,末藤大智,津田誠

    第22回次世代を担う若手のためのファーマ・バイオフォーラム  2023.9 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 脊髄後角アストロサイト―神経相互作用による新規痛覚制御メカニズム

    川邉陸,内山瑳和子,津田誠

    第22回次世代を担う若手のためのファーマ・バイオフォーラム2023  2023.9 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 神経障害性アロディニアに関与する脊髄後角興奮性神経の同定

    大西晃央,末藤大智,井絵理子,津田誠

    第42回鎮痛薬・オピオイドペプチドシンポジウム  2023.9 

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    Event date: 2024.4

    Language:Japanese  

    Country:Japan  

  • 痛覚伝達神経路におけるμオピオイド受容体恒常活性の短時間誘導法

    加納稜大、百木野和也、高露雄太、津田誠

    日本薬学会第143年会  2023.3 

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    Event date: 2023.3

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • 脊髄変化から紐解く痒みの慢性化機構 Invited

    白鳥美穂,津田誠

    第128回日本解剖学会総会・全国学術集会  2023.3 

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    Event date: 2023.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:仙台   Country:Japan  

  • 脊髄アストロサイトから紐解く感覚情報伝達の調節メカニズム Invited

    高露雄太、松田烈士、吉原康平、津田誠

    日本生理学会第100回記念大会  2023.3 

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    Event date: 2023.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Japan  

  • 痒み慢性化における脊髄後角の反応性アストロサイトの役割 Invited

    白鳥美穂、津田誠

    日本生理学会第100回記念大会  2023.3 

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    Event date: 2023.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Japan  

  • 神経とアストロサイトを介した脊髄ノルアドレナリンによる両方向性の疼痛調節

    津田誠,川邉陸,内山瑳和子,吉原康平

    第44回日本疼痛学会  2022.12 

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    Event date: 2022.12

    Language:Japanese  

    Venue:岐阜   Country:Japan  

  • 脊髄後角における非細胞自律的な体性感覚情報処理 Invited

    高露雄太、松田烈士、吉原康平、津田誠

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 脊髄後角ノルアドレナリンに関連した鎮痛効果に重要な脊髄後角抑制性神経サブセット

    末藤大智,石橋忠幸,吉川優,山浦健,津田誠

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • マウス外側腕傍核—扁桃体中心核痛み活性化ニューロン間シナプス伝達の痛み誘発増強

    内山瑳和子,奥田崇雄,高橋由香里,津田誠,加藤総夫

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 神経障害性アロディニアにおける大脳皮質-脊髄後角神経路の役割

    藤森一樹、津田誠

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • アストロサイト―神経相互作用を介した脊髄ノルアドレナリンによる双方向性痛覚制御

    川邉陸、吉原康平、津田誠

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 痒み伝達を担う脊髄神経サブセット Invited

    白鳥美穂、津田誠

    第96回日本薬理学会年会  2022.12 

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    Event date: 2022.11 - 2022.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 痛覚刺激によるμオピオイド受容体の恒常活性化の誘導

    加納稜大、百木野和也、高露雄太、津田誠

    第39回日本薬学会九州山口支部大会  2022.11 

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    Event date: 2022.11

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • 神経障害性アロディニアにおける大脳皮質-脊髄後角経路の役割

    藤森一樹、津田誠

    第39回日本薬学会九州山口支部大会  2022.11 

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    Event date: 2022.11

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • ミクログリアの組織内密度調節における機械感受性チャネルの役割

    山﨑絢斗、津田誠、増田隆博

    第75回日本薬理学会西南部会  2022.10 

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    Event date: 2022.10

    Language:Japanese  

    Venue:高知   Country:Japan  

  • α2δ-1 expressed in spinal dorsal horn excitatory neurons contributes to nerve injury-induced neuropathic pain

    Keisuke Koga, Kenta Kobayashi, Makoto Tsuda, Kazufumi Fubota, Yutaka Kitano, Hidemasa Furue

    Neuro2022  2022.6 

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    Event date: 2022.5 - 2022.6

    Language:English  

    Venue:沖縄   Country:Japan  

  • 出生後の脳境界マクロファージの定着にはIrf8およびMafbが関与する

    山崎絢斗,津田誠,増田隆博

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • 脊髄後角アストロサイトのαおよびβ受容体を介する異なる痛覚制御

    吉原康平,川邉陸,内山瑳和子,白坂亮二,古賀啓祐,津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • レセルピン誘発線維筋痛症モデルにおけるミクログリアの役割

    齊藤秀俊,細井昌子,津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • ストレス誘発性鎮痛におけるノルアドレナリンシグナルの関与

    内山瑳和子,吉原康平,川邉陸,古賀啓祐,津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • 神経障害性アロディニアに重要な脊髄後角抑制性神経の変化に対するアストロサイトの役割

    末藤大智,石橋忠幸,吉川優,山浦健,津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • ハイスループットスクリーニングにより新たに発見されたMRGPRA3アゴニストは引っ掻き行動を誘発する

    山下智大,伊藤麻結,川浪侑華,古賀啓介,兼久賢章,藤井志織,カアベイロホセ,津田誠

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡*ハイブリッド   Country:Japan  

  • 慢性ストレス誘発性痛覚過敏における脊髄後角アストロサイトサブセットを介したノルアドレナリン神経シグナルの役割

    吉原康平,津田誠

    第43回日本疼痛学会  2021.12 

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    Event date: 2021.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:愛知*オンライン   Country:Japan  

  • Aβ神経線維を介する神経障害性アロディニアに重要な脊髄後角サブセット

    末藤大智,石橋忠幸,吉川優,田島諒一,山浦健,津田誠

    第74回日本薬理学会西南部会  2021.11 

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    Event date: 2021.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:久留米   Country:Japan  

  • 痛覚を調節する脳-脊髄後角トップダウン神経路の網羅的解析

    藤森一樹,齊藤秀俊,勢力薫,橋本均,津田誠

    第74回日本薬理学会西南部会  2021.11 

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    Event date: 2021.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:久留米   Country:Japan  

  • ストレス誘発性鎮痛におけるノルアドレナリンシグナルの関与

    内山瑳和子,吉原康平,川邉陸,古賀啓祐,津田誠

    第38回日本薬学会九州山口支部大会  2021.11 

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    Event date: 2021.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:熊本*オンライン   Country:Japan  

  • 侵害刺激は下行性ノルアドレナリン神経シグナルを介して脊髄後角アストロサイトを活性化する

    川邉陸,吉原康平,津田誠

    第64回日本神経化学会大会  2021.9 

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    Event date: 2021.9 - 2021.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:奈良*オンライン   Country:Japan  

  • 慢性掻痒時のアストロサイトSTAT3の持続的活性化における一次求心性神経由来IL-6とIP3R1/TRPC依存的なカルシウムシグナルの関与

    白鳥美穂,山口千春,江口和志,豊永穂奈美,津田誠

    生体機能と創薬シンポジウム2020-2021  2021.8 

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    Event date: 2021.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:札幌*ハイブリッド   Country:Japan  

  • 青斑核由来下行性ノルアドレナリン神経による痒み抑制メカニズム

    白石悠人,古賀啓佑,白鳥美穂,津田誠

    生体機能と創薬シンポジウム2020-2021  2021.8 

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    Event date: 2021.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:札幌*ハイブリッド   Country:Japan  

  • 動物モデルを用いた心理社会的ストレスと痛みの科学的理解へのアプローチ Invited

    齊藤秀俊,津田誠

    第62回日本心身医学会総会ならびに学術講演会  2021.7 

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    Event date: 2021.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:高松   Country:Japan  

  • 神経障害性疼痛におけるミクログリアサブセットの役割

    河野敬太,津田誠

    日本薬学会第141年会  2021.3 

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    Event date: 2021.3

    Language:Japanese  

    Venue:広島*オンライン   Country:Japan  

  • 神経障害性疼痛回復期に出現するミクログリアサブポピュレーション

    河野敬太,津田誠

    第94回薬理学会年会  2021.3 

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    Event date: 2021.3

    Language:English  

    Venue:札幌*ハイブリッド   Country:Japan  

  • 侵害刺激による脊髄後角アストロサイトの活性化には下行性ノルアドレナリン神経シグナルが関与する

    川邉陸,吉原康平,津田誠

    第94回薬理学会年会  2021.3 

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    Event date: 2021.3

    Language:Japanese  

    Venue:札幌*ハイブリッド   Country:Japan  

  • 一次求心性神経由来NPTX2は脊髄後角GRPR陽性神経への興奮性シナプス入力の増大と慢性掻痒に関与する

    兼久賢章,津田誠

    第42回日本疼痛学会  2020.12 

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    Event date: 2020.12

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 脊柱管狭窄症由来の下肢痛における脊髄後角アストロサイトの役割

    大野瑛明,中島康晴,津田誠

    第42回日本疼痛学会  2020.12 

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    Event date: 2020.12

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 痒みにおける青斑核由来下行性ノルアドレナリン神経の役割

    白石悠人,古賀啓祐,白鳥美穂,津田誠

    第73日本薬理学会西南部会  2020.11 

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    Event date: 2020.11

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 脊柱管狭窄に伴う慢性疼痛発症における脊髄後角アストロサイトの役割

    大野瑛明,津田誠,中島康晴

    第35回日本整形外科学会基礎学術集会  2020.10 

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    Event date: 2020.10

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 脊柱管狭窄に伴う慢性疼痛発症における脊髄後角アストロサイトの役割

    大野瑛明,中島康晴,津田誠

    第63日本神経化学会大会  2020.9 

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    Event date: 2020.9

    Language:Japanese  

    Venue:オンライン   Country:Japan  

  • 脊髄後角アストロサイトを介した下行性ノルアドレナリン神経による新たな体性感覚制御メカニズム

    吉原康平,高露雄太,松田烈士,齊藤秀俊,井上和秀,津田誠

    第93回日本薬理学会年会  2020.3 

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    Event date: 2020.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • ノルアドレナリンによるミクログリアのインターロイキン1β産生はEPAC、MAP3K8によって調節される

    齊藤秀俊,笹木泉,山下智大,津田誠

    第93回日本薬理学会年会  2020.3 

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    Event date: 2020.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 新規MrgprA3アゴニストの発見およびかゆみ感覚に対するその評価

    山下智大,伊藤麻結,川浪侑華,古賀啓介,兼久賢章,藤井志織,白鳥美穂,津田誠

    第93回日本薬理学会年会  2020.3 

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    Event date: 2020.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • A subset of dorsal horn inhibitory interneurons has a critical role in mechanical allodynia after nerve injury Invited International conference

    Keisuke Koga, Ryoichi Tashima, Yuta Kohro, Kazuhide Inoue, Hiromu Yawo, Hidemasa Furue, Makoto Tsuda

    8th Asian pain symposium  2019.12 

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    Event date: 2019.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:Songdo   Country:Korea, Republic of  

  • 慢性掻痒時の活性化アストロサイトによる痒み増強メカニズム

    山方涼,古賀啓祐,白鳥美穂,津田誠

    第36回日本薬学会九州支部会  2019.11 

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    Event date: 2019.11

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • ミクログリアサブセットの神経障害性疼痛における新しい役割

    河野敬太、津田誠

    第72回日本薬理学会西南部会  2019.11 

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    Event date: 2019.11

    Language:Japanese  

    Venue:沖縄   Country:Japan  

  • 心理社会的ストレスが慢性疼痛病態モデルに及ぼす影響 Invited

    齊藤秀俊,津田誠

    第35回日本ストレス学会学術総会  2019.10 

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    Event date: 2019.10

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • Investigation of neuropathic allodynia with sensory and emotional components using an optogenetic approach International conference

    Makoto Tsuda, Ryoichi Tashima, Keisuke Koga, Hiromu Yawo, Hidemasa Furue

    第6回アジア神経精神薬理学会大会(AsCNP2019)  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • New role of a subset of spinal cord microglia in neuropathic pain International conference

    Keita Kohno, Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Papaverine potently activates MrgprA3 and produces scratching behavior International conference

    Tomohiro Yamashita, Mayu Ito, Yuka Kawanami, Keisuke Koga, Kensho Kanehisa, Shiori Fujii, Miho Shiratori-Hayashi, Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Sensitization of GRPR-expressing dorsal horn neurons under chronic itch condition requires astrocyte-derived signaling International conference

    Keisuke Koga, Ryo Yamagata, Miho Shiratori-Hayashi and Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Excitatory synaptic responses in GRPR+ dorsal horn neurons are increased in a mouse model of atopic dermatitis International conference

    Kensho Kanehisa, Keisuka Koga, Shiori Fujii, Miho Shiratori-Hayashi, Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Descending noradrenergic pathway modulates mechanosensory behavior via spinal dorsal horn astrocytes International conference

    Kohei Yoshihara, Yuta Kohro, Tsuyoshi Matsuda, Hidetoshi Tozaki-Saitoh, Verdon Taylor, Kazuhide Inoue, Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Mechanism underlying STAT3 activation in astrocytes under chronic itch conditions International conference

    Miho Shiratori-Hayashi, Chiharu Yamaguchi, Kazushi Eguchi, Honami Toyonaga, Makoto Tsuda

    THE 48th NAITO CONFERENCE  2019.10 

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    Event date: 2019.10

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • 慢性疼痛動物モデルの病態発症・維持機構に対するミクログリアの関与 Invited

    齊藤秀俊,津田誠

    日本線維筋痛症学会第11回学術集会  2019.10 

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    Event date: 2019.10

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • 慢性掻痒モデルマウスでは脊髄後角GRPR陽性神経への興奮性シナプス入力が増加する

    兼久賢章、古賀啓祐、白鳥美穂、津田誠

    生体機能とシンポジウム2019  2019.8 

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    Event date: 2019.8

    Language:Japanese  

    Venue:東京   Country:Japan  

  • Activated astrocytes in the spinal dorsal horn facilitate itch transmission in a mouse model of contact dermatitis

    Keisuke Koga, Ryo Yamagata, Miho Shiratori-Hayashi, Makoto Tsuda

    第42回日本神経科学大会,第62回日本神経化学会大会(Neuro2019)  2019.7 

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    Event date: 2019.7

    Language:Japanese  

    Venue:新潟   Country:Japan  

  • Social defeat stress modulates nocifensive response in remission phase of chronic pain models

    Hidetoshi Tozaki-Saitoh, Takuya Hatta, Makoto Tsuda

    第42回日本神経科学大会,第62回日本神経化学会大会(Neuro2019)  2019.7 

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    Event date: 2019.7

    Language:Japanese  

    Venue:新潟   Country:Japan  

  • 脊髄後角アストロサイトを介した下行性ノルアドレナリン神経による体性感覚制御

    吉原康平、高露雄太、松田烈士、齋藤秀俊、津田誠

    第41回日本疼痛学会  2019.7 

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    Event date: 2019.7

    Language:Japanese  

    Venue:名古屋   Country:Japan  

  • アトピー性皮膚炎モデルマウスにおける脊髄後角GRPR陽性神経への興奮性シナプス入力の増強

    兼久賢章,古賀啓祐,藤井志織,白鳥美穂,津田誠

    第41回日本疼痛学会  2019.7 

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    Event date: 2019.7

    Language:Japanese  

    Venue:名古屋   Country:Japan  

  • 心理社会的ストレスによる慢性疼痛の変調:ミクログリアの関与 Invited

    齊藤秀俊,津田誠

    第115回日本精神神経学会学術総会  2019.6 

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    Event date: 2019.6

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:新潟   Country:Japan  

  • Aβ線維を介する神経障害性アロディニアに関与する脊髄後角第II層神経サブセット

    津田誠,田島諒一,古賀啓祐

    第13回日本緩和医療薬学会年会  2019.6 

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    Event date: 2019.5 - 2019.6

    Language:Japanese  

    Venue:千葉   Country:Japan  

  • Aβ線維由来神経障害性アロディニアに関与する脊髄後角第II層神経サブセットの同定

    田島諒一,古賀啓祐,渡邊萌佳,関根美鈴,津田誠

    日本薬学会第139年会  2019.3 

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    Event date: 2019.3

    Language:Japanese  

    Venue:千葉   Country:Japan  

  • 脊髄後角アストロサイトの活性化は、接触性皮膚炎モデルマウスにおいて痒み伝達を増強する

    古賀啓祐,山方涼,白鳥美穂,津田誠

    第92回日本薬理学会年会  2019.3 

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    Event date: 2019.3

    Language:Japanese  

    Venue:大阪   Country:Japan  

  • アトピー性皮膚炎モデルマウスにおける脊髄後角GRPR陽性神経細胞への興奮性シナプス入力の増強

    兼久賢章,古賀啓祐,藤井志織,白鳥美穂,津田誠

    第92回日本薬理学会年会  2019.3 

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    Event date: 2019.3

    Language:Japanese  

    Venue:大阪   Country:Japan  

  • 転写因子MafBは脊髄ミクログリアの活性化と神経障害性疼痛に関与する

    齊藤秀俊、増田潤哉、米田聡介、小嶋ちなみ、川田竜、井上和秀、津田誠

    第92回日本薬理学会年会  2019.3 

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    Event date: 2019.3

    Language:Japanese  

    Venue:大阪   Country:Japan  

  • 乳がん治療薬フルベストラントはオキサリプラチン誘発末梢神経障害を抑制する

    山本将大,山下智大,伊藤麻結,ホセ・カーベイロ,江頭伸昭,齊藤秀俊,津田誠

    第92回日本薬理学会年会  2019.3 

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    Event date: 2019.3

    Language:Japanese  

    Venue:大阪   Country:Japan  

  • 神経障害性アロディニアに関与する一次求心性Aβ線維サブセット

    渡邊萌佳,田島諒一,関根美鈴,津田誠

    第35回日本薬学会九州支部大会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 一次求心性神経由来LGALS3の神経障害性疼痛および慢性掻痒病態への関与

    鷲頭加歩,河野敬太,白鳥美穂,津田誠

    第35回日本薬学会九州支部大会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛における脊髄ミクログリアの活性化タイムコース

    河野敬太,北野順子,高露雄太,齊藤秀俊,井上和秀,津田誠

    第35回日本薬学会九州支部大会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • アドレナリン受容体を介したミクログリアの炎症応答調節

    笹木泉、齊藤秀俊、津田誠

    第35回日本薬学会九州支部大会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 脊髄後角ミクログリアの転写因子MafBは末梢神経障害後の神経障害性疼痛発症に関与する

    齊藤秀俊、増田潤哉、川田竜、小嶋ちなみ、米田聡介、井上和秀、津田誠

    第35回日本薬学会九州支部大会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 感覚情報伝達における脊髄後角アストロサイト亜集団の役割

    高露雄太, 松田烈士, 吉原康平, 桂木龍一, 岡嵩晃, 田島諒一, 棟田翔, 山根拓也, 齊藤秀俊, 御子柴克彦, Verdon Taylor, 井上和秀, 津田誠

    第71回日本薬理学会西南部会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛寛解期の社会的敗北ストレス負荷は痛覚閾値の再低下を引き起こす

    齊藤秀俊,八田拓哉,井上和秀,津田誠

    第71回日本薬理学会西南部会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 脊髄後角GRPR陽性神経活動と慢性掻痒におけるアストロサイトの役割

    山方涼,古賀啓祐,白鳥美穂,津田誠

    第71回日本薬理学会西南部会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • ACSA2抗体を用いた脊髄アストロサイト単離法の確立

    山根拓也,高露雄太,津田誠

    第71回日本薬理学会西南部会  2018.11 

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    Event date: 2018.11

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • Sensitizing mechanosensory information by a population of spinal dorsal horn astrocytes International conference

    Yuta Kohro, Tsuyoshi Matsuda, Kohei Yoshihara, Ryuichi Katsuragi,Takaaki Oka, Sho Muneta, Ryoichi Tashima, Hidetoshi Tozaki-Saitoh, Katsuhiko Mikoshiba, Verdon Taylor, Kazuhide Inoue, Makoto Tsuda

    17th World Congress on Pain (IASP 2018)  2018.9 

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    Event date: 2018.9

    Language:Japanese  

    Venue:Boston   Country:Japan  

  • アロディニアの発症に関与する脊髄後角第II層神経サブポピュレーションの特定

    田島諒一,古賀啓祐,渡邊萌佳,関根美鈴,津田誠

    第17回 次世代を担う若手ファーマ・バイオフォーラム2018  2018.9 

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    Event date: 2018.9

    Language:Japanese  

    Venue:熊本   Country:Japan  

  • Rapid and selective inhibition of dorsal horn inhibitory interneurons induces morphine-resistant spontaneous nocifensive behaviors International conference

    Keisuke Koga, Kensho Kanehisa, Tozaki-Saitoh Hidetoshi, Hidemasa Furue, Makoto Tsuda

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  2018.7 

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    Event date: 2018.7

    Language:Japanese  

    Venue:京都   Country:Japan  

  • Social defeat stress arouses recurrence of pain in ameliorationg state International conference

    Hidetoshi Saitoh, Takuya Hatta, Kazuhide Inoue, Makoto Tsuda

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  2018.6 

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    Event date: 2018.7

    Language:Japanese  

    Venue:京都   Country:Japan  

  • Optogenetic activation of non-nociceptive Aβ fibers induces neuropathic pain-like sensory and emotional behaviors after nerve injury in rats International conference

    Ryoichi Tashima, Keisuke Koga, Misuzu Sekine, Kensho Kanehisa, Yuta Kohro, Yugo Fukazawa, Kazuhide Inoue, Hiromu Yawo, Hidemasa Furue, Makoto Tsuda

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  2018.7 

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    Event date: 2018.7

    Language:Japanese  

    Venue:京都   Country:Japan  

  • New pharmacological effects of approved drugs targeting P2X7 receptors against the release of IL-1β from microglial cells and neuropathic pain after peripheral nerve injury International conference

    Tomohiro Yamashita, Sawako Kamikaseda, Aya Tanaka, Hidetoshi Tozaki-Saitoh, Makoto Tsuda, Kazuhide Inoue

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  2018.7 

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    Event date: 2018.7

    Language:Japanese  

    Venue:京都   Country:Japan  

  • アロディニアの発症に関与する脊髄後角第II層神経サブポピュレーションの特定

    田島諒一,渡邊萌佳,関根美鈴,津田誠

    第40回日本疼痛学会  2018.6 

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    Event date: 2018.6

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • 脊髄後角アストロサイトを介したノルアドレナリンによる新しい感覚情報制御

    吉原康平,松田烈士,齊藤秀俊,高露雄太,津田誠

    日本薬学会第138年会  2018.3 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 転写因子MafBは末梢神経障害後の脊髄後角ミクログリアの活性化を調節し神経障害性疼痛に関与する

    齊藤秀俊,増田潤哉,小嶋ちなみ,米田聡介,川田竜,井上和秀,津田誠

    第39回日本疼痛学会  2017.6 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 脊髄後角抑制性介在神経の急性的な抑制はモルヒネ抵抗性の自発的疼痛関連行動を引き起こす

    古賀啓祐,兼久賢章,高露雄太,齋藤秀俊,井上和秀,古江秀昌,津田誠

    第39回日本疼痛学会  2017.6 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • D-セリンシグナルを介した脊髄後角アストロサイトによる触覚情報の変調作用

    高露雄太,桂木龍一,岡嵩晃,棟田翔,田島諒一,齊藤秀俊,御子柴克彦,井上和秀,津田誠

    第39回日本疼痛学会  2017.6 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • Specific activation of GABAergic interneurons in the cervical spinal dorsal horn suppresses chronic itch

    兼久賢章,白鳥美穂,古賀啓祐,高露雄太,津田誠

    第60回日本神経化学会大会  2017.9 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • The role of region-specific spinal dorsal horn astrocytes in sensory information processing

    高露雄太,桂木龍一,岡嵩晃,棟田翔,田島諒一,齊藤秀俊,井上和秀,津田誠

    第60回日本神経化学会大会  2017.9 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 頸部脊髄後角抑制性介在ニューロンの活性化による慢性的なかゆみの改善

    兼久賢章,白鳥美穂,古賀啓祐,高露雄太,津田誠

    第70回日本薬理学会西南部会  2017.11 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 脊髄後角アストロサイトの痛覚調節への関与

    吉原康平,松田烈士,齊藤秀俊,高露雄太,津田誠

    第70回日本薬理学会西南部会  2017.11 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 慢性掻痒に関与する脊髄後角神経伝達シグナル

    遠山かほり,白鳥美穂,津田誠

    第34回日本薬学会九州支部大会  2017.11 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 神経障害性アロディニアに関与する一次求心性Aβ線維:光遺伝学的解析

    関根美鈴,田島諒一,古賀啓祐,八尾寛,井上和秀,古江秀昌,津田誠

    第138回日本薬理学会関東部会  2018.3 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • 脊髄後角アストロサイトCa2+シグナルは感覚情報伝達に関与する

    松田烈士,吉原康平,齊藤秀俊,高露雄太,津田誠

    日本薬学会第138年会  2018.3 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • オキサリプラチン誘発末梢神経障害における脊髄グルタミン酸濃度の恒常性破綻と既承認薬リルゾールの保護効果

    山本将大,江頭伸昭,増田智先,津田誠

    日本薬学会第138年会  2018.3 

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    Event date: 2018.4

    Language:Japanese  

    Country:Japan  

  • デュロキセチンによるミクログリアに発現するP2X4受容体の阻害作用および末梢神経損傷に伴う神経障害性疼痛に対する改善効果

    山下 智大ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • 転写因子MafBは脊髄活性化ミクログリアに発現し神経障害性疼痛発症に関与する

    齊藤 秀俊ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • 慢性掻痒におけるアストロサイトSTAT3の活性化メカニズム

    山口千春ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • 頸髄後角の抑制性介在ニューロン活性化は接触性皮膚炎モデルにおける慢性掻痒を抑制する

    兼久 賢章ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • D-セリンシグナルを介した脊髄後角アストロサイトによる様式特異的な感覚情報処理への関与

    高露 雄太ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • MrgprA3陽性一次求心性神経に発現するP2X3受容体の活性化はGRP受容体依存的な痒みを発症する

    白鳥 美穂ら

    第90回日本薬理学会年会  2017.3 

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    Event date: 2017.3

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • Purinergic receptor P2X3 in MrgprA3-positive sensory neurons mediates the itch sensation through a pathway involving GRP receptors International conference

    Miho Shiratori-Hayashi et al.

    46th Annual Meeting Society for Neuroscience  2016.11 

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    Event date: 2016.11

    Language:English  

    Venue:San Diego   Country:United States  

  • Activation of spinal dorsal horn astrocytes modulates the processing of tactile sensation International conference

    Yuta Kohro et al.

    46th Annual Meeting Society for Neuroscience  2016.11 

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    Event date: 2016.11

    Language:English  

    Venue:San Diego   Country:United States  

  • 脊髄後角アストロサイトの活動変化は触覚情報を変調させる

    高露 雄太ら

    第60回日本神経化学会大会  2016.9 

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    Event date: 2016.9

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • DREADDを用いた脊髄アストロサイトの感覚情報伝達における機能解析

    高露 雄太ら

    第38回日本疼痛学会  2016.6 

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    Event date: 2016.6

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • パクリタキセル誘発末梢神経障害に対するポラプレジンクの効果

    堤国章ら

    日本薬学会第136年会  2016.3 

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    Event date: 2016.5

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • Role of STAT3-dependent reactive astrocytes in the spinal dorsal horn in chronic itch International conference

    白鳥 美穂ら

    XII European Meeting on Glial Cells in Health and Disease  2015.7 

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    Event date: 2016.5

    Language:English  

    Venue:Bilbao   Country:Spain  

  • P2X3R-positive sensory neurons are involved in itch sensation through a pathway involving GRP receptors International conference

    豊永穂奈美ら

    8th World Congress on Itch (WCI 2015)  2015.9 

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    Event date: 2016.5

    Language:English  

    Venue:nara   Country:Japan  

  • Astrocytic lipocalin-2 in the spinal dorsal horn is required for chronic itch International conference

    白鳥 美穂ら

    8th World Congress on Itch (WCI 2015)  2015.9 

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    Event date: 2016.5

    Language:English  

    Venue:nara   Country:Japan  

  • STAT3-dependent reactive astrocytes in the spinal dorsal horn contribute to the maintenance of chronic itch in mice International conference

    白鳥 美穂ら

    45th Annual Meeting Society for Neuroscience  2015.10 

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    Event date: 2016.5

    Language:English  

    Venue:Chicago   Country:United States  

  • 筋萎縮性側索硬化症治療薬リルゾールはオキサリプラチン誘発機械的アロディニアおよび脊髄グルタミン酸放出増加を抑制する

    山本将大ら

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.5

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • VGAT陽性脊髄後角抑制性介在ニューロンの抑制によって自発通関連行動が誘発される

    古賀啓祐ら

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.5

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 脊髄アストロサイトの活動変化は感覚情報を様式特異的に変調させる

    高露 雄太ら

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.5

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 脊髄後角におけるSTAT3依存的なアストロサイト活性化は痒みの慢性化に関与する

    白鳥 美穂ら

    日本薬学会第136年会  2016.3 

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    Event date: 2016.5

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 光遺伝学的手法を用いた一次求心性神経Aβ線維を介する神経障害性アロディニアの新規評価法

    田島諒一ら

    第89回日本薬理学会年会  2016.3 

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    Event date: 2016.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • 活性化ミクログリアにおける転写因子IRF1の役割

    御厨颯季ら

    第32回日本薬学会九州支部大会  2015.11 

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    Event date: 2015.11

    Language:Japanese  

    Venue:延岡   Country:Japan  

  • 光遺伝学的手法による神経障害性アロディニアの新規評価法

    田島諒一ら

    第68回日本薬理学会西南部会  2015.11 

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    Event date: 2015.11

    Language:Japanese  

    Venue:山口   Country:Japan  

  • アトピー性皮膚炎モデルマウスの慢性的な痒みにおける脊髄後角アストロサイトの関与

    津田 誠ら

    第45回日本神経精神薬理学会  2015.9 

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    Event date: 2015.9

    Language:Japanese  

    Venue:東京   Country:Japan  

  • Essential role for STAT3-dependent reactive astrocytes in maintenance of chronic itch

    白鳥 美穂ら

    第58回日本神経化学会大会  2015.9 

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    Event date: 2015.9

    Language:English  

    Venue:さいたま   Country:Japan  

  • In vivo Ca2+ imaging reveals that spinal astrocytes respond to nociceptor stimulation

    松田烈士ら

    第58回日本神経化学会大会  2015.9 

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    Event date: 2015.9

    Language:English  

    Venue:さいたま   Country:Japan  

  • 神経損傷後の一次求心性神経Aβ線維を介する疼痛関連行動:光遺伝学的アプローチを用いた神経障害性疼痛の新しい評価法

    田島諒一ら

    第37回日本疼痛学会  2015.7 

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    Event date: 2015.7

    Language:Japanese  

    Venue:熊本   Country:Japan  

  • ミクログリアに発現するP2X4 受容体を標的とした神経障害性疼痛治療薬の探索

    山下 智大ら

    日本薬学会第135年会  2015.3 

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    Event date: 2015.3

    Language:Japanese  

    Venue:神戸   Country:Japan  

  • ATP受容体を標的にしたエコファーマ~慢性疼痛の克服を目指して~ Invited

    津田 誠ら

    日本薬学会第135年会  2015.3 

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    Event date: 2015.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • アンメット・メディカル・ニーズの高い難治性疾患に対するアカデミック創薬:九州大学拠点の取り組み Invited

    津田 誠ら

    日本薬学会第135年会  2015.3 

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    Event date: 2015.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • ATP受容体を標的とした新規治療薬の探索に向けた新しい創薬システム「グリーンファルマ」の取り組み Invited

    山下 智大ら

    第8回次世代を担う若手医療薬科学  2014.11 

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    Event date: 2014.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:熊本   Country:Japan  

  • ATP受容体を標的とした新規治療薬の探索に向けた新しい創薬システム「グリーンファルマ」の取り組み Invited

    山下 智大ら

    第8回次世代を担う若手医療薬科学  2014.11 

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    Event date: 2014.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:熊本   Country:Japan  

  • ミクログリアの細胞膜P2X4受容体の発現制御に対するP2X7受容体の関与

    山下 智大, 津田 誠, 齊藤 秀俊, 井上 和秀

    日本薬学会第133回年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:横浜   Country:Japan  

  • パクリタキセル誘発慢性疼痛における脊髄内CCL3の関与

    落石龍太郎, 津田 誠, 永田健一郎, 矢野貴之, 井上智之, 齊藤 秀俊, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • スクリーニングシステムを利用したP2X4受容体を標的とした鎮痛薬の探索

    山下 智大, 長谷川あゆみ, 冨永桂子, 上加世田紗和子, 張佳明, 津田 誠, 齊藤 秀俊, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese  

    Venue:福岡   Country:Japan  

  • P2X4受容体のマイクログリア膜トラフィッキング制御 Invited

    Hidetoshi Saitoh, 津田 誠, 山下 智大, 井上 和秀

    第86回日本薬理学会年会  2013.3 

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    Event date: 2013.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • Role of P2X7 receptors in regulation of P2X4 receptors expression on the plasma membrane of microglia International conference

    山下 智大, TSUDA MAKOTO, Hidetoshi Saitoh, Kazuhide Inoue

    第55回日本神経化学会大会(APSN/JSN 2012)  2012.9 

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    Event date: 2012.9 - 2012.10

    Language:English  

    Venue:Kobe   Country:Japan  

  • Transcription factor MafB mediates activation process of spinal microglia that contributes to neuropathic pain development International conference

    Hidetoshi Saitoh, Junya Masuda, TSUDA MAKOTO, Kazuhide Inoue

    第55回日本神経化学会大会(APSN/JSN 2012)  2012.9 

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    Event date: 2012.9 - 2012.10

    Language:English  

    Venue:Kobe   Country:Japan  

  • DAP12およびCARD9ノックアウトマウスによる神経障害痛モデルの組織学的検討

    村田祐造, 八坂敏一, 原博満, 李明子, 藤田亜美, 津田 誠, 井上 和秀, 熊本栄一, 吉田裕樹, 増子貞彦

    第35回日本神経科学大会Neuro2012  2012.9 

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    Event date: 2012.9

    Language:Japanese  

    Venue:名古屋   Country:Japan  

  • 活性化ミクログリア細胞でのP2X7受容体によるP2X4受容体の細胞膜表面における発現レベルの調節

    山下 智大, 津田 誠, 齊藤 秀俊, 井上 和秀

    第34回日本疼痛学会  2012.7 

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    Event date: 2012.7

    Language:Japanese  

    Venue:熊本   Country:Japan  

  • Role of P2X7 Receptors in Regulation of P2X4 Receptors Expression on the Plasma Membrane of Microglia International conference

    山下智大, 津田 誠, Hidetoshi Saitoh, Kazuhide Inoue

    Purine 2012  2012.6 

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    Event date: 2012.5 - 2012.6

    Language:English  

    Venue:Fukuoka   Country:Japan  

  • CCL2 promotes P2X4 receptor trafficking to the cell surface of microglia Invited International conference

    Hidetoshi Saitoh, Emika Toyomitsu, TSUDA MAKOTO, 山下 智大, Yoshitaka Tanaka, Kazuhide Inoue

    Purine 2012  2012.5 

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    Event date: 2012.5 - 2012.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:Fukuoka   Country:Japan  

  • Involvement of Protein Kinase D in UDP-Induced Microglial Macropinocytosis and Phagocytosis International conference

    Ayumi Uesugi, Ayako Kataoka, Hidetoshi Saitoh, TSUDA MAKOTO, Kazuhide Inoue

    Purine 2012  2012.6 

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    Event date: 2012.5 - 2012.6

    Language:English  

    Venue:Fukuoka   Country:Japan  

  • デュロキセチンの神経障害性疼痛抑制メカニズムを考える Invited

    津田 誠

    第53回日本神経学会学術大会  2012.5 

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    Event date: 2012.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • ミクログリア活性化における転写因子MafBの役割

    米田聡介,齊藤秀俊,増田潤哉,津田誠,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Venue:京都市   Country:Japan  

  • ミクログリアの細胞膜P2X4受容体の発現制御に対するP2X7受容体の関与

    山下智大,津田誠,齊藤秀俊,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Venue:京都市   Country:Japan  

  • 神経障害性疼痛の緩和における脊髄CB2受容体の役割

    下山裕,増田隆博,吉永遼平,西本奈央,齊藤秀俊,津田誠,井上和秀

    第85回日本薬理学会年会  2012.3 

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    Event date: 2012.3

    Venue:京都市   Country:Japan  

  • 脊髄ミクログリア細胞から探る慢性疼痛メカニズム Invited

    津田誠,井上和秀

    第21回神経行動薬理若手研究者の集い  2012.3 

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    Event date: 2012.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:京都市   Country:Japan  

  • 神経障害性疼痛におけるミクログリアの転写因子MafBの役割

    米田聡介,増田潤哉,齊藤秀俊,津田 誠,井上和秀

    第39回薬物活性シンポジウム  2011.11 

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    Event date: 2011.11

    Venue:福岡県福岡市   Country:Japan  

  • 神経障害性疼痛におけるミクログリアP2Y12 受容体の関与

    齊藤秀俊,宮田広行,津田 誠,井上和秀

    第39回薬物活性シンポジウム  2011.11 

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    Event date: 2011.11

    Venue:福岡県福岡市   Country:Japan  

  • 神経障害性疼痛モデルにおいて脊髄ミクログリア特異的に発現する転写因子MafBの役割

    増田潤哉、齊藤秀俊、米田聡介、津田 誠、井上和秀

    第64回日本薬理学会西南部会  2011.11 

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    Event date: 2011.11

    Venue:福岡県福岡市   Country:Japan  

  • UDP誘発性のミクログリアによるマクロピノサイトーシスへのPKDの関与

    上杉歩未,片岡彩子,齊藤秀俊,津田誠,井上和秀

    第54回日本神経化学会大会  2011.9 

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    Event date: 2011.9

    Venue:石川県山代温泉   Country:Japan  

  • 初代培養ミクログリアにおけるP2Y12受容体を介したケモカインの発現制御

    齊藤秀俊,津田誠,井上和秀

    第54回日本神経化学会大会  2011.9 

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    Event date: 2011.9

    Venue:石川県山代温泉   Country:Japan  

  • Neuronal CCL21 up-regulates microglia P2X4 expression and initiates neuropathic pain development International conference

    Biber, K.; Tsuda, M.; Tozaki-Saitoh, H.; Tsukamoto, K.; Toyomitsu, E.; Masuda, T.; Boddeke, H.; Inoue, K

    10th Euroglia Meeting on Glial Cells in Health and Diseases  2011.9 

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    Event date: 2011.9

    Venue:Prague   Country:Czech Republic  

  • 初代培養ミクログリアにおけるP2Y12受容体を介したCCL3ケモカインの発現制御

    宮田広行,齊藤秀俊,津田誠,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • UDP刺激誘発性のミクログリア貪食におけるPKDの関与

    片岡彩子,上杉歩未,齊藤秀俊,津田誠,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • CTPによるミクログリアにおけるP2X4受容体の機能評価

    山下 智大, 津田 誠, 齊藤 秀俊, 井上 和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • 転写因子IRF8によるミクログリア遺伝子発現プログラムを介した神経障害性疼痛制御

    増田隆博,津田誠,吉永遼平,田村智彦,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • 神経障害性疼痛モデルマウスにおける活性化型脊髄ミクログリアは高い遊走能を有する

    増田潤哉,齊藤秀俊,津田誠,井上和秀

    第84回日本薬理学会年会  2011.3 

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    Event date: 2011.3

    Venue:横浜   Country:Japan  

  • 抗ラットP2X4抗体の調製とエピトープ解析

    井川達弘,阿部義人,東貞行,津田誠,井上和秀,植田正

    第27回日本薬学会九州支部大会  2010.12 

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    Event date: 2010.12

    Venue:長崎   Country:Japan  

  • Glial cells and pain control Invited

    Makoto Tsuda, Kazuhide Inoue

    Busan-Kyushu International Joint Seminar  2010.11 

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    Event date: 2010.11

    Presentation type:Symposium, workshop panel (public)  

    Venue:Pusan   Country:Korea, Republic of  

  • Glial cells and pain control Invited

    津田誠,井上和秀

    第15回グリア研究会  2010.10 

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    Event date: 2010.10

    Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛とミクログリアの活性化 Invited

    津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Japan  

  • Interferon regulatory factor-8はミクログリア由来疼痛関連分子の発現を誘導する転写因子である

    増田隆博,津田誠,吉永遼平,田村智彦,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • 神経障害性疼痛発症における脊髄CCL3の関与

    齊藤秀俊,津田誠,上田和明,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • 急性脳スライスにおけるミクログリアの状態のリアルタイムイメージング解析

    増田潤哉,齋藤秀俊,津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • CTPによるミクログリアにおけるP2X4受容体の機能評価

    山下智大,津田誠,齊藤秀俊,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • ミクログリアにおけるP2X7受容体活性化はNFATとPKC/MAPKを介してCXCL2産生に関与する

    白鳥美穂,齊藤秀俊,吉武麻衣,津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • UDPによるミクログリアの貪食促進作用におけるPKDの関与

    片岡彩子,齊藤秀俊,上杉歩未,古賀結衣,津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • 脊髄ミクログリアの活性化がパクリタキセル誘発機械刺激過敏、冷刺激過敏及び運動機能障害を引き起こす

    永田健一郎,井上智之,矢野貴之,高露雄太,大石了三,津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • 神経障害性疼痛の維持機構におけるSTAT3の役割

    高露雄太,津田誠,矢野貴之,辻川智子,北野順子,齊藤秀俊,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • 神経障害性疼痛の緩和における脊髄内CB2受容体とその下流メカニズムの重要性

    下山裕,塚本恵子,齊藤秀俊,津田誠,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • CCL2シグナルを介したフィブロネクチン刺激によるミクログリアP2X4受容体の膜移行

    豊満笑加,津田 誠,齊藤秀俊,井上和秀

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  2010.9 

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    Event date: 2010.9

    Venue:神戸   Country:Japan  

  • Spinal microglia: a key component in neuropathic pain Invited International conference

    Makoto Tsuda, Kazuhide Inoue

    The 13th Asian Australasian Congress of Anesthesiologists  2010.6 

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    Event date: 2010.6

    Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • Role of interferon regulatory factor-8 in the pathogenesis of neuropathic pain International conference

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Tomohiko Tamura, Kazuhide Inoue

    Purines 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Venue:Tarragona   Country:Spain  

  • CCR2 enhances P2X4 receptor trafficking to the plasma membrane of microglia International conference

    Emika Toyomitsu, Makoto Tsuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

    Purines 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Venue:Tarragona   Country:Spain  

  • Involvement of PKD in UDP-stimulated microglial phagocytosis International conference

    Ayako Kataoka, Hidetoshi Tozaki-Saitoh, Yui Koga, Ayumi Uesugi, Makoto Tsuda, Kazuhide Inoue

    Purines 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Venue:Tarragona   Country:Spain  

  • P2X7 receptor activation induces CXCL2 production in microglia through NFAT and PKC/MAPK pathways International conference

    Miho Shiratori, Hidetoshi Tozaki-Saitoh, Mai Yoshitake, Makoto Tsuda, Kazuhide Inoue

    Purines 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Venue:Tarragona   Country:Spain  

  • Analysis of microglial activation in tissue slice using two-photon imaging International conference

    Junya Masuda, Hidetoshi Tozaki-Saitoh, Makoto Tsuda, Kazuhide Inoue

    Purines 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Venue:Tarragona   Country:Spain  

  • 神経障害性疼痛におけるinterferon regulatory factor-8の役割

    増田隆博,津田誠,吉永遼平,田村智彦,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • UDP誘発ミクログリアの貪食反応におけるPKDの関与

    片岡彩子,齊藤秀俊,古賀結衣,上杉歩未,津田誠,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • CCL2はミクログリア細胞膜上でのP2X4受容体発現を増加する

    豊満笑加,津田誠,山下智大,齊藤秀俊,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • 神経障害性疼痛発症時の脊髄CCL3の関与

    齊藤秀俊,上田和明,津田誠,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • UDP誘発性ミクログリア貪食作用におけるVASPリン酸化の関与

    古賀結衣,片岡彩子,齊藤秀俊,津田誠,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • ミクログリア貪食時における一過性のカルシウム上昇

    齊藤秀俊,津田誠,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • ミクログリアからのATP誘発CXCL2放出メカニズム

    白鳥美穂,齊藤秀俊,吉武麻衣,津田誠,井上和秀

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Venue:大阪   Country:Japan  

  • 神経障害性疼痛治療薬としてのミクログリア活性化阻害剤 Invited

    井上和秀,津田誠

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Japan  

  • ミクログリアからのATP誘発CXCL2放出メカニズム

    白鳥美穂,齊藤秀俊,吉武麻衣,津田誠,井上和秀

    第62回日本薬理学会西南部会  2009.11 

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    Event date: 2009.11

    Venue:愛媛・松山   Country:Japan  

  • 神経障害性疼痛の維持におけるSTAT3の役割

    高露雄太,津田誠,矢野貴之,辻川智子,北野順子,齊藤秀俊,井上和秀

    第62回日本薬理学会西南部会  2009.11 

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    Event date: 2009.11

    Venue:愛媛・松山   Country:Japan  

  • 脊髄CB2受容体の活性化による神経因性疼痛抑制メカニズム

    下山裕,塚本恵子,齊藤秀俊,津田誠,井上和秀

    第3回次世代を担う若手医療薬科学シンポジウム  2009.11 

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    Event date: 2009.11

    Venue:福岡   Country:Japan  

  • 抗うつ薬による神経因性疼痛寛解作用とそのメカニズムの解析

    米谷美穂,松村祐太,永田健一郎,津田誠,井上和秀

    第3回次世代を担う若手医療薬科学シンポジウム  2009.11 

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    Event date: 2009.11

    Venue:福岡   Country:Japan  

  • Glial Function and pain signaling Invited International conference

    Makoto Tsuda, Kazuhide Inoue

    Kyushu Brain days  2009.11 

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    Event date: 2009.11

    Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • 脊髄ミクログリア活性化と神経因性疼痛 Invited

    井上和秀,津田誠

    第31回日本疼痛学会 / 名古屋ペイン2009  2009.7 

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    Event date: 2009.7

    Presentation type:Oral presentation (general)  

    Venue:愛知・名古屋   Country:Japan  

  • 脊髄CB2受容体の活性化による神経因性疼痛抑制メカニズム

    下山裕,津田誠,齊藤秀俊,井上和秀

    第31回日本疼痛学会 / 名古屋ペイン2009  2009.7 

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    Event date: 2009.7

    Venue:名古屋   Country:Japan  

  • 血小板由来増殖因子PDGF誘発アロディニアにおける脊髄ミクログリアの関与

    増田潤哉,津田誠,齊藤秀俊,井上和秀

    第52回日本神経化学会大会  2009.6 

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    Event date: 2009.6

    Venue:群馬   Country:Japan  

  • フィブロネクチン刺激ミクログリアにおけるP2X4受容体発現増加の翻訳および翻訳後制御

    豊満笑加,津田誠,齊藤秀俊,井上和秀

    第52回日本神経化学会大会  2009.6 

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    Event date: 2009.6

    Venue:群馬   Country:Japan  

  • 神経因性疼痛に重要な脊髄後角ミクログリアの活性化メカニズム Invited

    津田誠,増田隆博,井上和秀

    第18回神経行動薬理若手研究者の集い  2009.3 

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    Event date: 2009.3

    Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • 末梢神経損傷によるCa2+/カルモジュリン依存性プロテインキナーゼIIを介した細胞質型ホスホリパーゼA2の活性化

    長谷川茂雄,高露雄太,津田誠,井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Venue:横浜   Country:Japan  

  • 神経損傷による脊髄アストロサイトの活性化と神経因性疼痛に対するSTAT3の役割

    辻川智子、津田誠、矢野貴之、井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Venue:横浜   Country:Japan  

  • 脊髄における血小板由来増殖因子PDGFはミクログリアのPDGF受容体を介してアロディニアを発現する

    増田潤哉,津田誠,齊藤秀俊,井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Venue:横浜   Country:Japan  

  • 末梢神経損傷により脊髄および後根神経節において増加するCB2受容体のCB2作動薬誘発抗アロディニア効果における役割

    下山裕,津田誠,塚本恵子,齊藤秀俊,井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Venue:横浜   Country:Japan  

  • 神経損傷による脊髄アストロサイトの活性化とその神経因性疼痛に対する役割

    辻川智子,津田誠,井上和秀

    第61回日本薬理学会西南部会  2008.11 

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    Event date: 2008.11

    Venue:鳥取   Country:Japan  

  • ミクログリアからのATP 誘発MIP-2 放出のメカニズム

    吉武麻衣,齊藤秀俊,白鳥美穂,津田誠,井上和秀

    第61回日本薬理学会西南部会  2008.11 

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    Event date: 2008.11

    Venue:鳥取   Country:Japan  

  • Platelet-activating factor receptor is required for production of proinflammatory cytokines and neuropathic pain after nerve injury International conference

    Shigeo Hasegawa, Makoto Tsuda and Kazuhide Inoue

    38th Annual Meeting Society for Neuroscience  2008.11 

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    Event date: 2008.11

    Venue:DC   Country:United States  

  • Interferon-γ and Lyn tyrosine kinase are required for spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    Takahiro Masuda, Makoto Tsuda and Kazuhide Inoue

    38th Annual Meeting Society for Neuroscience  2008.11 

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    Event date: 2008.11

    Venue:DC   Country:United States  

  • P2Y6-evoked microglial phagocytosis Invited International conference

    K. Inoue, S. Koizumi, M. Tsuda

    XI WORKSHOP ON APOPTOSIS IN BIOLOGY AND MEDICINE  2008.9 

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    Event date: 2008.9

    Presentation type:Oral presentation (general)  

    Venue:仙台   Country:Japan  

  • Interferon-γ receptors are required for spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    Makoto Tsuda, Takahiro Masuda, Kazuhide Inoue

    The 3rd International Conference of Neurons and Brain Disease  2008.8 

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    Event date: 2008.8

    Venue:Seoul   Country:Korea, Republic of  

  • フィブロネクチンによるミクログリアP2X4受容体発現増加におけるp53の役割

    豊満笑加,津田誠,米谷美穂,齊藤秀俊,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • 末梢神経損傷によるミクログリアの活性化と神経因性疼痛発症におけるIFN-γの役割

    増田隆博,津田誠,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • 神経因性疼痛における血小板活性化因子受容体の役割

    長谷川茂雄,津田誠,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • ミクログリアからのATP誘発ケモカイン放出におけるNFATの関与

    片岡彩子,齊藤秀俊,古賀結衣,津田誠,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • triply-NOS欠損マウスでの神経因性疼痛の緩和とミクログリアの活性化の抑制

    久保山和哉,津田誠,齊藤秀俊,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • 神経因性疼痛における脊髄ミクログリアP2Y12受容体の関与

    齊藤秀俊,津田誠,井上和秀

    第30回日本疼痛学会 / 福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Role of platelet-activating factor receptor in neuropathic pain International conference

    Shigeo Hasegawa, Makoto Tsuda, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Involvement of NFAT in chemokine release from microglia induced by ATP International conference

    Ayako Kataoka, Yui Koga, Makoto Tsuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Reduced spinal microglia activation and neuropathic pain after nerve injury in mice lacking all three nitric oxide synthases International conference

    Kazuya Kuboyama, Makoto Tsuda, Masato Tsutsui, Yumiko Toyohira, Hidetoshi Tozaki-Saitoh, Hiroaki Shimokawa, Nobuyuki Yanagihara, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Role of interferon-gamma in spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    Takahiro Masuda, Makoto Tsuda, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Role of p53 in microglial P2X4 receptor upregulation by fibronectin International conference

    Emika Toyomitsu, Makoto Tsuda, Miho Kometani, Hidetoshi Saitoh, Kazuhide Inoue

    The 3rd Asian Pain Symposium  2008.7 

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    Event date: 2008.7

    Venue:福岡   Country:Japan  

  • Interferon-γ receptor regulates spinal microglia activation and neuropathic pain after nerve injury

    井上和秀,増田隆博,津田誠

    日本神経科学会  2008.7 

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    Event date: 2008.7

    Venue:東京   Country:Japan  

  • Lynチロシンキナーゼは神経因性疼痛を引き起こすIFN-γ依存的なミクログリアの活性化に必須である

    増田隆博,津田誠,井上和秀

    第82回日本薬理学会年会  2009.3 

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    Event date: 2008.3 - 2009.3

    Venue:横浜   Country:Japan  

  • 低侵襲的な脊髄後角へのマイクロインジェクション法を用いた細胞種および部位特異的な遺伝子導入

    高露 雄太ら

    第88回日本薬理学会年会  2015.3 

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    Language:Japanese  

    Venue:名古屋   Country:Japan  

  • Astrocytic STAT3 is a crucial factor for reactive astrocytes after nerve injury and neuropathic pain

    高露 雄太ら

    Neuro2013  2013.6 

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    Language:Japanese  

    Venue:京都   Country:Japan  

  • Chronic pain increases neurokinin 1 receptor mRNA expression in the bed nucleus of stria terminalis: Roles of neurokinin 1 receptor in the anxiety-like behavior

    眞嶋悠幾ら

    Neuro2013  2013.6 

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    Language:Japanese  

    Venue:京都   Country:Japan  

  • Role of IRF5 in P2X4R upregulation in microglia and neuropathic pain

    津田 誠ら

    Neuro2013  2013.6 

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    Language:Japanese  

    Venue:京都   Country:Japan  

  • Transcription factor MafB mediates activation process of spinal microglia that contributes to neuropathic pain development

    齊藤 秀俊ら

    Neuro2013  2013.6 

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    Language:Japanese  

    Venue:京都   Country:Japan  

  • 神経障害性疼痛におけるアストロサイトSTAT3シグナルの役割

    高露 雄太ら

    生体機能と創薬シンポジウム  2013.8 

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    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 神経障害性疼痛に重要な脊髄ミクログリアの活性化分子メカニズム Invited

    津田 誠

    第28回日本整形外科学会基礎学術集会  2013.10 

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    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:千葉   Country:Japan  

  • 転写因子IRF5は脊髄ミクログリアP2X4受容体の発現増加を介して神経障害性疼痛発症維持に関与する

    岩本祥佑ら

    第66回日本薬理学会西南部会  2013.11 

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    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 神経障害後の脊髄ミクログリアにおけるMafB発現誘導メカニズムの解析

    小嶋ちなみ ら

    第66回日本薬理学会西南部会  2013.11 

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    Language:Japanese  

    Venue:福岡   Country:Japan  

  • 脊髄後角におけるSTAT3依存的なアストロサイト活性化は慢性的な痒みに必要である

    白鳥美穂ら

    第87回日本薬理学会年会  2014.3 

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    Language:English  

    Venue:仙台   Country:Japan  

  • 末梢神経損傷後に活性化する脊髄ミクログリアへの骨髄由来細胞の寄与

    冨山大輔ら

    第87回日本薬理学会年会  2014.3 

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    Language:Japanese  

    Venue:仙台   Country:Japan  

  • ケモカイン受容体CCR5の神経障害性疼痛への関与

    松下克之ら

    第87回日本薬理学会年会  2014.3 

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    Venue:仙台   Country:Japan  

  • IRF5は神経障害性疼痛を誘発するP2X4受容体発現ミクログリアを直接制御している

    増田 隆博ら

    第87回日本薬理学会年会  2014.3 

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    Venue:仙台   Country:Japan  

  • Transcriptional regulation of microglial motility by IRF8

    松田烈志ら

    第87回日本薬理学会年会  2014.3 

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    Venue:仙台   Country:Japan  

  • 転写因子IRF8-IRF5軸は神経障害性疼痛を誘発するP2X4受容体発現ミクログリアを制御している

    増田 隆博ら

    日本薬学会第134年会  2014.3 

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    Language:Japanese  

    Venue:熊本   Country:Japan  

  • 神経障害性疼痛発症における脊髄VNUTの役割

    増田 隆博ら

    第36回日本疼痛学会  2014.6 

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    Language:Japanese  

    Venue:大阪   Country:Japan  

  • ラット脊髄後角表層GABAニューロンへの興奮性シナプス入力に対するP2X3受容体の役割

    古賀啓祐ら

    第36回日本疼痛学会  2014.6 

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    Language:Japanese  

    Venue:大阪   Country:Japan  

  • アデノ随伴ウイルスによる脊髄アストロサイト特異的遺伝子導入法を用いた神経障害性疼痛の解析

    高露 雄太ら

    第130回日本薬理学会関東部会  2014.7 

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    Language:Japanese  

    Venue:東京   Country:Japan  

  • 転写因子IRF5は神経障害性疼痛を誘発するP2X4受容体高発現ミクログリアを制御している

    増田 隆博ら

    第130回日本薬理学会関東部会  2014.7 

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    Language:Japanese  

    Venue:東京   Country:Japan  

  • VNUT contributes to the pathogenesis of neuropathic pain after nerve injury International conference

    Masuda Takahiro et al.

    Purines2014  2014.7 

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    Language:English  

    Venue:Bonn   Country:Germany  

  • Searching for analgesics targeted at P2X4 receptors by screening of well-established drugs International conference

    Tomohiro Yamashita et al.

    Purines2014  2014.7 

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    Venue:Bonn   Country:Germany  

  • VNUT is required for the pathogenesis of neuropathic pain after nerve injury

    増田 隆博ら

    第36回日本生物学的精神医学会・第57回日本神経化学会大会合同大会  2014.9 

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    Language:Japanese  

    Venue:奈良   Country:Japan  

  • Duloxetine inhibits P2X4 receptor-mediated calcium responses and suppresses neuropathic pain in rats

    Jiaming Zhangら

    第8回次世代を担う若手医療薬科学  2014.11 

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    Venue:熊本   Country:Japan  

  • IRF5 is a crucial determinant for the formation of P2X4R+ reactive microglia driving neuropathic pain International conference

    Masuda Takahiro et al.

    44th Annual Meeting Society for Neuroscience  2014.11 

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    Language:English  

    Venue:Washington DC   Country:United States  

  • Spinal astrocytic STAT3 is a crucial factor for reactive astrocytes in neuropathic pain International conference

    Yuta Kohro et al.

    44th Annual Meeting Society for Neuroscience  2014.11 

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    Language:English  

    Venue:Washington DC   Country:United States  

  • ミクログリアに発現するP2X4受容体を標的とした神経障害性疼痛治療薬の探索に向けたエコファーマの取り組み

    山下 智大ら

    第67回日本薬理学会西南部会  2014.11 

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    Language:Japanese  

    Venue:北九州   Country:Japan  

  • 侵害刺激時における脊髄アストロサイトシグナリングのin vivo imaging

    松田烈士ら

    第67回日本薬理学会西南部会  2014.11 

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    Venue:北九州   Country:Japan  

  • 神経障害性疼痛モデルマウスの脊髄内におけるATP放出量の増加とVNUTの役割

    大園由衣ら

    第67回日本薬理学会西南部会  2014.11 

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    Venue:北九州   Country:Japan  

  • P2X3受容体を介した、脊髄後角抑制性介在ニューロンの興奮性シナプス伝達の調節

    古賀啓祐ら

    第67回日本薬理学会西南部会  2014.11 

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    Venue:北九州   Country:Japan  

  • 痒み発症における一次求心性神経P2X3受容体の関与

    白鳥 美穂ら

    第67回日本薬理学会西南部会  2014.11 

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    Venue:北九州   Country:Japan  

  • 脊髄後角抑制性介在ニューロンの興奮性シナプス伝達に対するP2X3受容体の役割

    古賀啓祐ら

    第31回日本薬学会九州支部大会  2014.12 

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    Venue:福岡   Country:Japan  

  • VNUTは神経障害性疼痛発症に重要な役割を果たしている

    増田 隆博ら

    第88回日本薬理学会年会  2015.3 

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    Venue:名古屋   Country:Japan  

  • 神経損傷によるミクログリア活性化と神経因性疼痛におけるIFN-gの役割

    増田隆博,津田誠,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • フィブロネクチンにより誘発される脊髄ミクログリアP2X4受容体発現亢進と神経因性疼痛

    小泉修一,多田薫,津田 誠,国房恵巳子,井上和秀

    第79回日本神経科学大会  2006.7 

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  • 脊髄後角でのニューロンとグリア細胞の相互作用による神経興奮の長期増強

    池田 弘,津田 誠,井上和秀,村瀬一之

    第28回日本疼痛学会  2006.7 

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  • Inhibitory effects of antidepressants on P2X4 receptor: a novel mechanism in neuropathic pain relief

    永田健一郎,津田誠,井上和秀

    第49回日本神経化学会大会  2006.9 

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    Country:Japan  

  • Activation of spinal microglia in diabetic neuropathic pain rats

    上野光,津田誠,井上和秀

    第49回日本神経化学会大会  2006.9 

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    Country:Japan  

  • Fibronectin increases expression of P2X4 receptors via ERK activation in microglia

    豊満笑加,津田誠,井上和秀

    第49回日本神経化学会大会  2006.9 

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  • インターフェロン-γ髄腔内投与は脊髄ミクログリアの活性化および持続性異痛症を引き起こす

    増田隆博,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • 抗うつ薬のP2X4受容体阻害作用:神経因性疼痛寛解作用メカニズムとしての可能性

    永田健一郎,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • 脊髄内ミクログリアにおけるERKの活性化は糖尿病誘発アロディニアに関与する

    上野光,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • フィブロネクチンによるミクログリアP2X4受容体発現増加の分子メカニズム

    豊満笑加,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • 神経因性疼痛におけるATP受容体を介した細胞質型ホスホリパーゼA2の活性化

    長谷川茂雄,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • ラット海馬アストロサイトからのIL-6放出とATP受容体との関連

    藤田拓美,津田誠,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • 神経因性疼痛におけるSrcファミリーチロシンキナーゼLynの役割

    津田誠,増田隆博,手塚徹,北野順子,山本雅,井上和秀

    第80回日本薬理学会年会  2007.3 

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  • ATP receptor-dependent neuropathic pain: a mechanism of the modulation of pain sensation Invited International conference

    K. Inoue, M. Tsuda, H. Saitoh-Tozaki

    7th IBRO World Congress of Neuroscience  2007.7 

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    Presentation type:Symposium, workshop panel (public)  

    Venue:Melbourne   Country:Australia  

  • UDP, a novel mediator of microglia phagocytosis Invited

    小泉修一,最上由香里,多田薫,篠崎陽一,大澤圭子,津田 誠,高坂新一,井上和秀

    第50回日本神経化学会大会 / Neuro2007  2007.9 

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    Country:Japan  

  • Involvement of NFAT in chemokine release from microglia induced by ATP

    片岡彩子,津田誠,井上和秀

    第50回日本神経化学会大会 / Neuro2007  2007.9 

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    Venue:横浜   Country:Japan  

  • Minocycline attenuates spinal microglia activation and tactile allodynia caused by interferon-γ

    増田隆博,津田誠,井上和秀

    第50回日本神経化学会大会 / Neuro2007  2007.9 

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  • 神経因性疼痛動物モデルにおける脊髄内ミクログリア増殖様式の解明

    北野順子,津田誠,辻川智子,井上和秀

    第60回日本薬理学会西南部会  2007.11 

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    Venue:宮崎   Country:Japan  

  • UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis International conference

    Koizumi S, Shigemoto-Mogami Y, Nasu-Tada K, Shinozaki Y, Ohsawa K, Tsuda M, Joshi BV, Jacobson KA, Kohsaka S, Inoue K

    37th Annual Meeting Society for Neuroscience  2007.11 

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    Venue:San Diego   Country:United States  

  • Role of purinergic signaling in IL-6 release from cultured rat hippocampal astrocytes International conference

    Fujita T, Tsuda M, Inoue K

    37th Annual Meeting Society for Neuroscience  2007.11 

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    Venue:San Diego   Country:United States  

  • Intrathecal administration of interferon-γ produces spinal microglia activation and long-lasting tactile allodynia International conference

    Masuda T, Tsuda M, Shimoyama H, Inoue K

    37th Annual Meeting Society for Neuroscience  2007.11 

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    Venue:San Diego   Country:United States  

  • ミクログリアにおけるP2X4受容体の発現および分布に対するラフトマイクロドメインの関与

    岡綾香、津田誠、齊藤秀俊、井上和秀

    第60回日本薬理学会西南部会  2007.11 

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    Venue:宮崎   Country:Japan  

  • 脊髄におけるアロデニアのメカニズム Invited International conference

    津田誠

    第1回学際的に痛みを考える会-国際フォーラムMusculoskeletal Pain Research-  2007.12 

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    Presentation type:Oral presentation (general)  

    Country:Japan  

  • 「私を食べてシグナル」UDPとミクログリアの貪食作用 Invited

    小泉修一,最上由香里,多田薫,篠崎陽一,大澤圭子,津田誠,高坂新一,井上和秀

    第81回日本薬理学会年会  2008.3 

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    Country:Japan  

  • ミクログリアからのATP誘発ケモカイン放出におけるNFAT関与

    片岡彩子,齊藤秀俊,古賀結衣,津田誠,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • 神経因性疼痛発症過程におけるP2Y12受容体の関与

    齊藤秀俊,津田誠,宮田広行,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • 海馬アストログリアおよび神経細胞の酸化ストレス障害に対するATPの防御機能

    藤田拓美,齊藤秀俊,津田誠,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • フィブロネクチンによるミクログリアP2X4受容体発現増加におけるp53の役割

    豊満笑加,津田誠,米谷美穂,齊藤秀俊,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • Triply-NOS欠損マウスでの神経因性疼痛の緩和とミクログリアの活性化の抑制

    久保山和哉,津田誠,筒井正人,豊平由美子,齊藤秀俊,下川宏明,柳原延章,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • 神経因性疼痛発症過程における脊髄フィブロネクチンの役割

    小松孝行,津田誠,山本希美子,安藤譲二,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • フィブロネクチンによるミクログリアP2X4受容体のラフトマイクロドメインへの移行

    岡綾香,津田誠,齊藤秀俊,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • 後根神経節の血小板活性化因子受容体は神経因性疼痛に関与する

    長谷川茂雄,津田誠,石井聡,清水孝雄,井上和秀

    第81回日本薬理学会年会  2008.3 

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  • (基礎系)神経内分泌と知覚 痒み感覚の神経伝達機構と皮膚炎による変化

    津田 誠

    日本内分泌学会雑誌  2024.4  (一社)日本内分泌学会

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  • 「神経再生・修復の最新知見」 神経障害に伴う慢性疼痛の発症・維持機構

    津田 誠

    脳循環代謝  2023.11  (一社)日本脳循環代謝学会

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  • グリア機能のデコーディング-脳の生理と病態の理解を目指して 痛覚伝達変調におけるグリア細胞の役割

    津田 誠

    臨床神経学  2022.10  (一社)日本神経学会

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  • 痛みと痒みの新解釈:病態メカニズムと脳機能修飾の統合理解への挑戦 脊髄アストロサイト集団を介した下行性疼痛制御機構の新たな役割

    高露 雄太, 津田 誠

    日本神経精神薬理学会年会プログラム・抄録集  2023.9  (一社)日本神経精神薬理学会

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  • 痛みの慢性化と緩和に関わるグリア細胞

    津田 誠

    日本ペインクリニック学会誌  2023.6  (一社)日本ペインクリニック学会

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  • 神経とアストロサイトを介した脊髄ノルアドレナリンによる両方向性の疼痛調節

    津田 誠, 川邉 陸, 内山 瑳和子, 吉原 康平

    PAIN RESEARCH  2022.12  (一社)日本疼痛学会

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  • 神経・グリアクロストークが織りなす神経病態 ミクログリアから見た神経損傷による痛みの慢性化機序

    津田 誠

    The Journal of Toxicological Sciences  2024.7  (一社)日本毒性学会

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  • 神経障害性アロディニアに直結する脊髄後角抑制性神経の活動低下には活性化アストロサイトが必要である

    末藤 大智, 石橋 忠幸, 吉川 優, 山浦 健, 津田 誠

    PAIN RESEARCH  2024.11  (一社)日本疼痛学会

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  • 神経障害性疼痛における脊髄後角神経に発現するα2δ-1サブユニットの役割

    古賀 啓祐, 小林 憲太, 津田 誠, 窪田 一史, 北野 裕, 古江 秀昌

    PAIN RESEARCH  2023.12  (一社)日本疼痛学会

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  • 神経障害性疼痛機序から考えられる新たな治療法の可能性を探る

    津田 誠

    日本ペインクリニック学会誌  2022.6  (一社)日本ペインクリニック学会

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  • 胎児期に腎腫大を伴う羊水過小を呈した常染色体顕性多嚢胞性腎の一例

    須郷 秀雄, 篠原 拓実, 加藤 舞, 渥美 優志, 西田 安里, 吉田 凪子, 渋井 亮介, 津田 誠, 岡田 智志, 片岡 史夫, 進 伸幸, 永松 健, 潮見 隆之

    千葉県産科婦人科医学会雑誌  2025.1  (一社)千葉県産科婦人科医学会

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  • 脊髄のCD11c陽性ミクログリアを増加させることで神経障害性疼痛を緩和に導く

    河野 敬太, 白坂 亮二, 津田 誠

    PAIN RESEARCH  2024.11  (一社)日本疼痛学会

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  • 身体不活動は,神経原性炎症と脊髄-外側腕傍核-扁桃体経路の活性化を通じて,広範囲機械痛覚過敏,触覚アロディニア,冷痛覚過敏に寄与する

    大道 裕介, 大道 美香, 田島 諒一, 大須賀 浩二, Kanikowska Dominika, 深澤 有吾, 八尾 寛, 津田 誠

    金沢医科大学雑誌  2023.12  金沢医科大学医学会

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  • 非神経細胞疼痛ネットワーク研究のプレビジョン 青斑核ノルアドレナリン神経 脊髄後角アストロサイト連関による痛覚変調機構

    津田 誠

    PAIN RESEARCH  2024.11  (一社)日本疼痛学会

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▼display all

MISC

  • Microglial diversity in neuropathic pain Invited Reviewed

    Tsuda M, Masuda T, Kohno K

    Trends Neurosci   46   597 - 610   2023.7

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  • 痛みと痒みの慢性化メカニズムに関する最新知見

    津田誠

    臨床麻酔   2023.3

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  • 神経障害性疼痛の寛解および再発に関与する脊髄ミクログリア集団

    津田誠

    化学工業   2023.1

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  • ミクログリアと慢性疼痛 ~新しいステージへ~ Reviewed

    津田誠

    実験医学   2022.11

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  • 脊髄後角アストロサイトサブセットを介するノルアドレナリン痛覚伝達制御

    津田誠

    麻酔科プラクティス   2022.11

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  • 慢性疼痛とミクログリア ~新たな方向性~

    津田誠

    麻酔71   2022.11

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  • 中枢神経系の慢性炎症と痛み

    津田誠

    ペインクリニック   2022.5

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  • 神経系マクロファージによる痛覚変調

    津田誠

    実験医学40(5), 108-113, 2022   2022.3

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  • Spinal glial cells in itch modulation Reviewed

    Shiatori-Hayashi M, Tsuda M

    Pharmacol Res Perspect   2021.12

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  • 痒みとグリア細胞

    津田誠

    日本医師会雑誌   2021.11

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  • グリア細胞が作り出す神経機能異常による痛みや痒み

    津田誠

    生体の科学   2021.10

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  • アストロサイトと神経障害性疼痛

    津田誠

    実験医学   2021.9

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  • 脊髄後角

    津田誠

    医学のあゆみ   2021.7

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  • 脊髄後角での痛覚信号プロセシングとグリア細胞

    津田誠

    BRAIN and NERVE   2021.7

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  • かゆみにおけるグリア細胞の働き Reviewed

    津田誠

    実験医学   2021.2

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  • Role of microglia and P2X4 receptors in chronic pain Reviewed

    Kohno K, Tsuda M

    Pain Rep   2021.1

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  • マウス脊髄後角の細胞を標的とした遺伝子導入法 Reviewed

    高露雄太,津田誠

    実験医学別冊「決定版 ウイルスベクターによる遺伝子導入実験ガイド」平井宏和,日置寛之,小林和人/編   2020.11

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  • マウス脊髄後角の細胞を標的とした遺伝子導入法

    高露雄太,津田誠

    実験医学別冊   2020.11

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  • Role of reactive astrocytes in the spinal dorsal horn under chronic itch conditions Reviewed

    Shiratori-Hayashi M, Tsuda M

    J Pharmacol Sci   2020.11

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  • グリア細胞による痒みの慢性化機構 Reviewed

    津田誠

    ファルマシア   2020.9

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  • グリア細胞による痛覚の調節機構 Reviewed

    津田誠

    実験医学   2020.2

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  • Microglia-Mediated Regulation of Neuropathic Pain: Molecular and Cellular Mechanisms Reviewed

    Makoto Tsuda

    2019.12

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    DOI: 10.1248/bpb.b19-00715

  • New approach for investigating neuropathic allodynia by optogenetics

    Tsuda M

    Pain   2019.5

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    DOI: 10.1097/j.pain.0000000000001506

  • Microglia-mediated regulation of neuropathic pain Molecular and cellular mechanisms Reviewed

    Makoto Tsuda

    Biological and Pharmaceutical Bulletin   2019.1

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    Pain is a defense system that responds rapidly to harmful internal and external stimuli through the somatosensory neuronal pathway. However, damage to the nervous system through cancer, diabetes, infection, autoimmune disease, chemotherapy or trauma often leads to neuropathic pain, a debilitating chronic pain condition. Neuropathic pain is not simply a temporal continuum of acute nociceptive signals from the periphery, but rather due to pathologically altered functions in the nervous system, which shift the net neuronal excitatory balance toward excitation. Although alterations were long thought to be a result of changes in neurons, but an increasing body of evidence over the past decades indicates the necessity and sufficiency of microglia, the tissue-resident macrophages of the spinal cord and brain, for nerve injury-induced malfunction of the nervous system. In this review article, I describe our current understanding of the molecular and cellular mechanisms underlying the role of microglia in the pathogenesis of neuropathic pain and discuss the therapeutic potential of microglia from recent advances in the development of new drugs targeting microglia.

    DOI: 10.1248/bpb.b19-00715

  • Microglia in neuropathic pain: cellular and molecular mechanisms and therapeutic potential.

    Inoue K, Tsuda M

    Nat Rev Neurosci   2018.3

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    Acute nociceptive pain is a key defence system that enables the detection of danger signals that threaten homeostasis and survival. However, chronic pain (such as the neuropathic pain that occurs after peripheral nerve injury) is not simply a consequence of the continuity of acute nociceptive signals but rather of maladaptive nervous system function. Over recent decades, studies have provided evidence for the necessity and sufficiency of microglia for the alterations in synaptic remodelling, connectivity and network function that underlie chronic pain and have shed light on the underlying molecular and cellular mechanisms. It is also becoming clear that microglia have active roles in brain regions important for the emotional and memory-related aspects of chronic pain. Recent advances in the development of new drugs targeting microglia and the establishment of new sources of human microglia-like cells may facilitate translation of these findings from bench to bedside.

    DOI: 10.1038/nrn.2018.2

  • Microglial regulation of neuropathic pain

    TSUDA MAKOTO et al.

    J Pharmacol Sci   2013.10

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  • Microglia and intractable chronic pain

    TSUDA MAKOTO, Beggs S, Salter MW, Kazuhide Inoue

    Glia   2013.1

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  • 末梢神経損傷による神経障害性疼痛とグリア

    津田 誠, 齊藤 秀俊, 井上 和秀

    Brain and Nerve   2012.11

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  • Purinergic system, microglia and neuropathic pain.

    Tsuda M, Tozaki-Saitoh H, Inoue K.

    Curr Opin Pharmacol.   2012.2

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  • Microglia and neuropathic pain.

    Inoue K, Tsuda M

    Glia   2009.11

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  • 慢性疼痛における細胞外ヌクレオチドとその受容体の役割

    津田 誠,井上和秀

    生化学   2009.10

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  • 神経障害性疼痛におけるATP受容体の役割

    津田誠,齊藤秀俊,井上和秀

    ペインクリニック別冊春号   2009.4

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  • 脊髄ミクログリアを介する神経因性疼痛の発症維持メカニズム

    津田誠

    神経化学,46(4),820-826(2007)   2007.12

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  • Neuropathic pain and spinal microglia: a big problem from molecules in "small" glia.

    Tsuda M, Inoue K, Salter MW.

    Trends Neurosci. 2005 Feb;28(2):101-7.   2005.2

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  • Astrocytic GPR37L1: A new guardian against the onset and chronicity of neuropathic pain

    Kohro Y., Tsuda M.

    Neuron   113 ( 8 )   1121 - 1123   2025.4   ISSN:08966273

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    In this issue of Neuron, Xu et al.1 demonstrate that activating GPR37L1, a G-protein-coupled receptor that negatively regulates astrocytes, suppresses the onset and maintenance of neuropathic pain, an intractable chronic pain caused by nerve damage, thereby serving as a therapeutic target.

    DOI: 10.1016/j.neuron.2025.03.013

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  • 【疼痛の制御】ミクログリアによる疼痛制御

    津田 誠

    Medical Science Digest   50 ( 8 )   418 - 421   2024.7   ISSN:1347-4340

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    がんや糖尿病,帯状疱疹など神経障害を伴う多くの疾患では,末梢組織への刺激に相応しない痛みが慢性的に現れる。例えば,通常よりも痛みが強まる痛覚過敏や,触刺激でも痛みが生じるアロディニアが挙げられる。この原因として,体性感覚伝達系の機能異常の関与が提唱されているが,その異常にはグリア細胞が重要な役割を担う。特に,末梢神経の損傷後早期に脊髄後角で活性化するミクログリアは,炎症性サイトカインや神経栄養因子などを産生放出し,神経の機能異常を導き,神経障害性疼痛の発症を引き起こす。さらに最近,活性化したミクログリアの一部が,異なる遺伝子発現パターンを有するサブセットに変化し,それが疼痛症状の寛解に必要であることも明らかになった。これらの知見より,ミクログリアは神経損傷後に遺伝子発現や機能をダイナミックに変化させ,慢性疼痛の発症と寛解にそれぞれ重要な役割を担うことが示唆されている。(著者抄録)

  • 【Glia・glymphatic systemと神経疾患】痛覚伝達におけるグリア細胞の役割

    津田 誠

    脳神経内科   101 ( 1 )   21 - 26   2024.7   ISSN:2434-3285

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  • ミクログリアの多様性から読み解く神経障害性疼痛

    津田誠,河野敬太

    日本薬理学雑誌   2024.4

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  • 【痛覚変調性疼痛の神経メカニズム】新たな下行性疼痛制御のメカニズム

    津田 誠

    ペインクリニック   45 ( 3 )   263 - 269   2024.3   ISSN:0388-4171

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    青斑核(LC)のノルアドレナリン(NA)神経は,恐怖や不安,覚醒,ストレス,そして痛覚調節などに関与する.脊髄へ投射する下行性LC-NA神経は,痛覚伝達を抑制性に制御するとされてきたが,最近筆者らは,脊髄後角の表層に限局したアストロサイトサブセットが下行性LC-NA神経からのNAシグナルを受容し,軽度機械刺激に対する痛覚過敏を引き起こすことを明らかにした.本稿では,この痛覚伝達を促進性に制御するという,下行性LC-NA神経の新しい調節機構について概説する.(著者抄録)

  • 慢性疼痛とアロスタシス:グリア細胞の役割

    1. 津田誠

    BRAIN and NERVE   2023.11

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  • 神経障害性疼痛の慢性化を抑止する新たな細胞

    津田誠

    Clinical Neuroscience   2023.11

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  • ニューロサイエンスの最新情報 神経障害性疼痛の慢性化を抑止する新たな細胞

    津田 誠

    Clinical Neuroscience   41 ( 11 )   1520 - 1521   2023.11   ISSN:0289-0585

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  • 【アロスタシス-ホメオスタシスを超えて】慢性疼痛とアロスタシス グリア細胞の役割

    津田 誠

    BRAIN and NERVE: 神経研究の進歩   75 ( 11 )   1225 - 1229   2023.11   ISSN:1881-6096

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    <文献概要>体性感覚神経系の傷害や疾患によって神経障害性疼痛という慢性疼痛が発症する。最近,この慢性疼痛モデルマウスを用いた研究から,神経損傷後に脊髄で出現するCD11c陽性ミクログリアが疼痛症状の寛解に重要な細胞として特定された。本論では,神経損傷後のミクログリアの状態変遷と,CD11c陽性ミクログリアによる神経障害性疼痛に対するアロスタティックな制御機構について概説する。

  • 【痒み】痒みと掻破の悪循環の神経系における分子メカニズム

    津田 誠

    皮膚科   4 ( 3 )   280 - 286   2023.9   ISSN:2436-570X

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  • 【ミクログリアがコードする情報の読み出しへの挑戦】ミクログリアの多様性から読み解く神経障害性疼痛

    津田 誠, 河野 敬太

    日本薬理学雑誌   158 ( 5 )   362 - 366   2023.9   ISSN:0015-5691

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    体性感覚神経系の傷害や疾患によって神経障害性疼痛という慢性疼痛が発症する.病態モデル等を用いたこれまでの研究から,神経障害性疼痛の発症におけるミクログリアの寄与が示されてきた.神経損傷等を感知したミクログリアは,細胞形態や遺伝子発現を伴いその細胞機能を変化させ,痛覚伝達神経の興奮性を高めて疼痛の発症を誘導する.しかし最近,神経障害性疼痛の寛解期に増加するミクログリアサブセット(CD11c陽性)が新たに特定され,疼痛の自然寛解に必要であることと,その後も寛解状態の維持に重要な役割を担うことが明らかになった.すなわち,神経損傷によって変化したミクログリアの機能や役割は一元的ではなく,発症・維持・寛解という各フェーズにおいてダイナミックに変化することが示唆される.これらのミクログリアの多様性とその役割に関する新しい知見から,神経障害性疼痛や他の神経疾患を読み解く新しいストラテジーの確立が期待される.(著者抄録)

  • 痒みの抑制機構 Reviewed

    白鳥美穂,津田誠

    Monthly Book Derma   2023.7

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  • 【痒みのサイエンス】痒みの抑制機構

    津田 誠

    Derma.   ( 337 )   25 - 30   2023.7   ISSN:1343-0831

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    皮膚や粘膜から発生した痒み信号は神経を介して脊髄と脳へ伝達されて痒みを感じる.近年の研究から,脊髄と脳には痒み信号を選択的に処理・統合・出力する回路が存在することが示されている.神経系の機能は,興奮性と抑制性シグナルのバランスによって調節されている.痒みの神経伝達機構においても例外ではなく,痒み信号の伝達に重要な脊髄後角神経(ガストリン放出ペプチド受容体発現神経)の活動を抑える抑制性介在神経サブセットが特定されている.また,脳幹から脊髄後角へ投射する下行性神経からのセロトニンやノルアドレナリンシグナルなども痒み神経伝達抑制機構として重要な役割を担っている.本稿では,痒みシグナルの神経伝達に対して抑制的に制御する脊髄後角神経および脳からの下行性神経に焦点を絞り,その神経化学的メカニズムについて概説する.(著者抄録)

  • Function of Glial Cells in Neuroinflammatory and Neuroimmunological Responses II

    Afridi R., Bhusal A., Tsuda M., Ryu H., Suk K.

    Cells   12 ( 13 )   2023.7

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    DOI: 10.3390/cells12131750

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  • ミクログリア細胞から慢性疼痛のメカニズムを紐解く

    津田誠

    日本心療内科学会誌   2023.6

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  • ミクログリア細胞から慢性疼痛のメカニズムを紐解く

    津田 誠

    日本心療内科学会誌   27 ( 2 )   84 - 90   2023.6   ISSN:1342-9558

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    痛みは,有害な刺激から身を守るために必要な感覚であるが,身体や精神的要因によって大きく変化する。例えば,がんや糖尿病,帯状疱疹治癒後など神経障害を伴う多くの疾患では,通常よりも痛みが強まり(痛覚過敏),触刺激でも痛みが生じてしまう(アロディニア)。このような末梢組織への刺激に相応しない痛みの原因として,グリア細胞による中枢神経ネットワーク機能異常が注目されている。脊髄では,神経損傷に応答してミクログリアが活性化し,それが産生放出する炎症性サイトカインや神経栄養因子などが神経の動作異常を引き起こす。さらに最近,活性化したミクログリアの一部が,異なる遺伝子発現パターンを有するサブセットに変化し,それが痛覚過敏行動の寛解に必要であることが判明した。すなわち,ミクログリアは神経損傷後に遺伝子発現や機能をダイナミックに変化させ,慢性疼痛の発症と寛解にそれぞれ重要な役割を担うことが示唆される。(著者抄録)

  • The Functions and Phenotypes of Microglia in Alzheimer’s Disease Reviewed

    Fujikawa R, Tsuda M

    Cells   2023.4

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  • The Functions and Phenotypes of Microglia in Alzheimer’s Disease Reviewed

    Fujikawa R, Tsuda M

    Cells   12   1207   2023.4

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  • 慢性疼痛とミクログリア 新たな方向性

    津田 誠

    麻酔   71 ( 増刊 )   S91 - S97   2022.11   ISSN:0021-4892

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  • 【脳をしなやかに制御するミクログリアと脳内免疫系 見えてきた起源と多様性、創薬標的の可能性】ミクログリアと慢性疼痛 新しいステージへ

    津田 誠

    実験医学   40 ( 18 )   2944 - 2949   2022.11   ISSN:0288-5514

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    体性感覚神経系の傷害や疾患によって神経障害性疼痛が発症する.この慢性疼痛には,痛覚情報伝達系の神経とそれらのネットワークの異常が関与する.そのしくみはいまだ解明されていないが,神経の傷害等に伴って活性化するミクログリアが異常を起こす原因であることがわかってきた.さらに最近,活性化したミクログリアのなかに,疼痛を緩和させる作用を有するサブセットが発見され,慢性疼痛における同細胞のダイナミックな変化と新しい役割が明らかになった.本稿では,これらに関するこれまでの流れと最近の成果をもとに,現時点で想定される最新のメカニズムを概説する.(著者抄録)

  • Author Correction: Specification of CNS macrophage subsets occurs postnatally in defined niches (Nature, (2022), 604, 7907, (740-748), 10.1038/s41586-022-04596-2)

    Masuda T., Amann L., Monaco G., Sankowski R., Staszewski O., Krueger M., Del Gaudio F., He L., Paterson N., Nent E., Fernández-Klett F., Yamasaki A., Frosch M., Fliegauf M., Bosch L.F.P., Ulupinar H., Hagemeyer N., Schreiner D., Dorrier C., Tsuda M., Grothe C., Joutel A., Daneman R., Betsholtz C., Lendahl U., Knobeloch K.P., Lämmermann T., Priller J., Kierdorf K., Prinz M.

    Nature   610 ( 7930 )   E1   2022.10   ISSN:00280836

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    In the version of this article initially published online, there was a copy– paste duplication of values in the source data for Figure 1b, Parenchyma: Cx3cr1-GFP+. The correct values have been restored in the HTML version of this article.

    DOI: 10.1038/s41586-022-05361-1

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  • 【脳-腸連関と慢性痛・慢性疾患】中枢神経系の慢性炎症と痛み

    津田 誠

    ペインクリニック   43 ( 5 )   490 - 496   2022.5   ISSN:0388-4171

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    近年の研究から、神経系における慢性炎症環境が慢性痛の発症に密接に関わることが示されている。中枢神経系においては、ミクログリアやアストロサイトなどのグリア細胞が炎症環境の誘導と維持の中核を成す。また、これらのグリア細胞は、中枢神経系内でのシグナルのみならず、腸などの末梢臓器からのシグナルによっても大きく影響を受けることが最近の研究から明らかになってきた。そこで本稿では、グリア細胞を介する脳と脊髄での慢性炎症と慢性痛の関係性について概説する。(著者抄録)

  • 【シン・マクロファージ あらゆる疾患を制御する機能的多様性】(第2章)病気とマクロファージの多様性を知る14の方法 神経系マクロファージによる痛覚変調

    津田 誠

    実験医学   40 ( 5 )   744 - 749   2022.3   ISSN:0288-5514

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    皮膚などの末梢組織から発生する侵害受容信号は神経を介して脳まで伝達されるが、その信号は非神経細胞からのシグナルによって大きく変調することがわかってきた。特に、一次求心性神経での末梢性感作、および脊髄後角と脳での中枢性感作は慢性疼痛の原因として有力視されているが、その感作機構にマクロファージ・ミクログリアが重要な役割を担う。本稿では、一次求心性神経、脊髄後角および脳におけるマクロファージ・ミクログリアの役割に関する成果および現在想定されるメカニズムを概説する。(著者抄録)

  • 神経障害性疼痛の新しい分子病態

    津田誠

    Precision Medicine   2022.2

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  • cutting-edge medicine 痛みの精密医療の展開に向けて 神経障害性疼痛の新しい分子病態

    津田 誠

    Precision Medicine   5 ( 2 )   105 - 108   2022.2   ISSN:2434-3625

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  • 神経障害性疼痛のメカニズム

    津田誠

    ペインクリニック   2021.5

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  • グリア細胞とかゆみ

    白鳥美穂,津田誠

    Medical Science Digest   2021.4

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  • 一次求心性神経Aβ線維由来の神経障害性アロディニアに重要な脊髄後角神経サブセット Reviewed

    津田誠

    日本運動器疼痛学会誌   2021.4

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  • Chronic itchとアストロサイト

    津田誠

    臨床免疫・アレルギー科   2021.2

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  • Nociceptive signaling mediated by P2X3, P2X4 and P2X7 receptors Reviewed

    Inoue K, Tsuda M

    Biochem Pharmacol   2021.1

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  • ノルアドレナリンによる痛覚制御機構:グリア細胞を介する新しいメカニズム

    津田誠

    日本生物学的精神医学会誌   2021.1

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  • 脊髄におけるmicrogliaによる中枢感作形成

    津田誠

    ペインクリニック   2020.12

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  • ミクログリアと神経障害性疼痛 Reviewed

    津田誠

    医学のあゆみ   2020.6

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  • Microglia-neuron interactions in the models of neuropathic pain Reviewed

    Hidetoshi Tozaki-Saitoh, Makoto Tsuda

    Biochemical Pharmacology   2019.11

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    Chronic pain is a debilitating condition that often emerges as a clinical symptom of inflammatory diseases. It has therefore been widely accepted that the immune system critically contributes to the pathology of chronic pain. Microglia, a type of immune cell in the central nervous system, has attracted researchers’ attention because in rodent models of neuropathic pain that develop strong mechanical and thermal hypersensitivity, histologically activated microglia are seen in the dorsal horn of spinal cord. Several kinds of cytokines are generated by damaged peripheral neurons and contribute to microglial activation at the distal site of the injury where damaged neurons send their projections. Microglia are known as key players in the surveillance of the local environment in the central nervous system and have a significant role of circuit remodeling by physical contact to synapses. Key molecules for the pathology of neuropathic pain exist in the activated microglia, but the factors driving pain-inducible microglial activation remain unclear. Therefore, to find the key molecules inducing activation of spinal microglia and to figure out the precise mechanism of how microglia modulate neuronal circuits in the spinal cord to form chronic pain state is a critical step for developing effective treatment of neuropathic pain.

    DOI: 10.1016/j.bcp.2019.08.016

  • 痛みと痒みの慢性化とグリア細胞 Reviewed

    津田誠

    実験医学   2019.10

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  • 神経障害による痛み Reviewed

    津田誠

    あたらしい眼科   2019.6

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  • ニューロパシックペインの発症・維持の機序について Reviewed

    津田誠

    ペインクリニック   2019.5

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  • 感覚情報処理における脊髄グリア細胞の役割

    津田誠

    日本顎関節学会誌   2019.4

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  • 脊髄後角での基礎研究

    津田誠

    ペインクリニック   2019.1

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  • 脊髄後角の神経・グリア相互作用が作り出す慢性掻痒

    津田誠

    PAIN RESEARCH   2018.12

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  • 神経障害性疼痛と神経系マクロファージ

    津田誠

    実験医学   2018.9

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  • 痒みのメカニズム:痒みの慢性化と脊髄後角アストロサイト

    津田誠

    神経内科   2018.7

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  • 目の前のチャンスに気付けるか

    津田誠

    日本薬理学雑誌   2018.7

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  • 痛みと中枢神経系免疫細胞

    津田誠

    炎症と免疫   2018.7

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  • 脊髄後角アストロサイトと掻痒

    津田誠

    臨床免疫・アレルギー科   2018.4

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  • 痛みが慢性化する神経メカニズム:特にニューロン-グリア連関の関与について

    津田誠

    ペインクリニック   2018.4

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  • Astrocytes in the spinal dorsal horn and chronic itch.

    Tsuda M

    2018.2

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    DOI: 10.1007/s12264-017-0129-y

  • 5. Nishimura A, Sunggip C, Oda S, Numaga-Tomita T, Tsuda M, Nishida M

    Nishimura A, Sunggip C, Oda S, Numaga-Tomita T, Tsuda M, Nishida M

    Pharmacol Ther   2017.12

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    DOI: 10.1016/j.pharmthera.2017.06.010

  • 慢性化したかゆみのメカニズム

    白鳥美穂、津田誠

    Visual Dermatology   2017.11

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  • P2 receptors, microglial cytokines and chemokines, and neuropathic pain

    TSUDA MAKOTO

    J Neurosci Res 95(6): 1319-1329   2017.6

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  • Purinergic P2Y6 receptors: A new therapeutic target of age-dependent hypertension.

    Sunggip C, Nishimura A, Shimoda K, Numaga-Tomita T, Tsuda M, Nishida M

    Pharmacol Res   2017.6

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    DOI: 10.1016/j.phrs.2017.03.013

  • Spinal dorsal horn astrocytes: new players in chronic itch

    TSUDA MAKOTO

    Allergol Int 66: 31-35   2017.1

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  • 脊髄では何がおきているのか? : 神経障害性疼痛の脊髄後角におけるメカニズム

    津田 誠

    医学のあゆみ 260(2), 141-143   2017.1

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  • 慢性炎症と痒み

    津田 誠

    最新医学71, 114-118   2016.11

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  • ATP受容体

    津田 誠

    White 4, 152-155   2016.11

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  • 慢性的なかゆみの新しい神経系メカニズム

    津田 誠, 白鳥 美穂

    生化学 88(5), 654-656   2016.10

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  • 脊髄後角アストロサイトと痒み

    津田 誠

    アレルギー・免疫23(9), 1200-1205   2016.9

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  • 神経障害性疼痛の発症維持メカニズム

    津田 誠

    ファルマシア   2016.8

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  • ミクログリアと神経障害性疼痛

    増田隆博ら

    細胞 48(8), 357-360   2016.8

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  • 慢性痛とグリア細胞

    齊藤 秀俊ら

    Clinical Neuroscience   2016.8

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  • P2Y受容体(ATP受容体)関連分子をターゲットとした臨床応用

    齊藤 秀俊ら

    Clinical Neuroscience   2016.7

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  • P2Y 受容体(ATP 受容体)の生理的および薬理的作用

    齊藤 秀俊ら

    Clinical Neuroscience   2016.6

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  • 慢性的な痒みにおけるSTAT3依存的な活性化アストロサイトの役割

    白鳥 美穂, 津田 誠

    臨床免疫・アレルギー科65(5), 458-462   2016.5

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  • Neuron-microglia interaction by purinergic signaling in neuropathic pain following neurodegeneration

    TSUDA MAKOTO et al.

    Neuropharmacology, 104:76-81   2016.5

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  • Transcriptional regulation in microglia and neuropathic pain

    Masuda T et al.

    Pain Manag. 6(2): 91-94   2016.4

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  • ミクログリアの活性化と形質を制御するIRF転写因子ファミリー

    増田隆博ら

    生化学   2016.2

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  • 脊髄後角におけるSTAT3依存的なアストロサイト活性化は痒みの慢性化に必要である

    白鳥 美穂ら

    実験医学   2016.1

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  • 痒みの伝達とその慢性化の神経系メカニズム

    津田 誠

    感染 炎症 免疫   2016.1

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  • アトピー性皮膚炎に伴う慢性的な痒みと脊髄後角アストロサイト

    津田 誠

    生体の科学   2015.12

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  • 痛覚

    津田 誠

    Clinical Neuroscience   2015.5

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  • P2Y 受容体(ATP 受容体)の種類

    齊藤 秀俊ら

    Clinical Neuroscience   2015.5

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  • 脊髄内痛み物質同定のためのマイルストーン研究

    津田 誠

    Pain Research   2015.3

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  • グリア細胞から見た神経障害性疼痛メカニズム

    津田 誠

    日本神経精神薬理学雑誌   2015.2

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  • 神経障害性疼痛

    津田 誠, 松下克之, 井上 和秀

    日本薬理学雑誌   2014.4

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  • 慢性疼痛におけるグリア細胞の関与と治療応用への可能性

    津田 誠, 井上 和秀

    臨床整形外科   2013.12

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  • 慢性疼痛におけるグリア細胞の関与と治療応用への可能性

    津田 誠ら

    臨床整形外科   2013.10

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  • Microglial regulation of neuropathic pain

    TSUDA MAKOTO, Masuda Takahiro, Hidetoshi Saitoh, Kazuhide Inoue

    J Pharmacol Sci   2013.2

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  • 慢性難治性疼痛とミクログリア活性化

    井上 和秀, 津田 誠, 齊藤 秀俊, 増田 隆博

    炎症と免疫   2012.11

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  • P2X4 receptors of microglia in neuropathic pain

    Kazuhide Inoue, TSUDA MAKOTO

    CNS Neurol Disord Drug Targets   2012.9

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  • Purinergic systems, neuropathic pain and the role of microglia.

    Inoue K, Tsuda M.

    Exp Neurol.   2012.4

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  • Role of purinergic receptors in CNS function and neuroprotection.

    Tozaki-Saitoh H, Tsuda M, Inoue K

    Adv Pharmacol   2011.9

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  • 痛みの分子メカニズムにおける最近の話題

    津田 誠,井上和秀

    化学と生物   2011.8

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  • Platelet-activating factor and pain.

    Tsuda M, Tozaki-Saitoh H, Inoue K

    Biol Pharm Bull.   2011.7

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  • P2Y6-evoked microglial phagocytosis

    Inoue K, Koizumi S, Kataoka A, Tozaki-Saitoh H, Tsuda M

    Int Rev Neurobiol   2010.7

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  • Pain and purinergic signaling.

    Tsuda M, Tozaki-Saitoh H, Inoue K

    Brain Res Rev   2010.5

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  • 痛みの慢性化と脊髄グリア細胞の役割

    津田誠,井上和秀

    臨床麻酔   2010.3

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  • 高速原子間力顕微鏡を用いた受容体の1分子イメージング

    篠崎陽一、住友弘二、津田 誠、小泉修一、井上和秀、鳥光慶一

    日本薬理学雑誌   2009.8

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  • ATP受容体

    井上和秀、津田誠、斎藤秀俊

    Clinical Neuroscience   2009.5

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  • 痛みとATP受容体

    井上和秀,津田誠,斎藤秀俊

    ペインクリニック   2009.3

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  • 鎮痛薬開発の現状とこれから

    津田 誠,井上和秀

    月刊薬事   2008.11

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  • 神経障害性疼痛におけるATP受容体の役割

    津田誠,齊藤秀俊,井上和秀

    ペインクリニック,29(2),164-169(2008)   2008.2

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  • The role of nucleotides in the neuron–glia communication responsible for the brain functions

    Inoue K, Koizumi S, Tsuda M

    J Neurochem 102: 1447–1458 (2007)   2007.9

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  • 神経因性疼痛と脊髄ミクログリアのATP受容体

    津田誠,井上和秀:

    BRAIN and NERVE-神経研究の進歩,59,953-959(2007)   2007.9

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  • Modification of neuropathic pain sensation through microglial ATP receptors

    Kazuhide Inoue, Makoto Tsuda, Hidetoshi Tozaki-Saitoh

    Purinergic Signalling, 3: 311-316 (2007)   2007.9

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  • ATP受容体を介する慢性疼痛発症機構

    津田誠,井上和秀

    医学のあゆみ 222,892-893 (2007)   2007.9

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  • P2Y12受容体を介するミクログリア細胞運動

    津田誠

    日本薬理学雑誌129, 389 (2007)   2007.5

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  • 脊髄ミクログリアのATP受容体を介する新しい神経因性疼痛メカニズム

    津田誠

    日本薬理学雑誌129, 349-353 (2007)   2007.5

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  • 神経およびグリア細胞培養系を利用した疼痛基礎研究

    津田誠,長谷川茂雄,小泉修一,井上和秀

    ペインクリニック, 27, 1597-1604 (2006)   2006.12

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  • 細胞外ATPを介した表皮ケラチノサイトー知覚神経間コミュニケーション;痛み伝達への関与

    小泉修一,藤下加代子,津田誠,井上和秀

    Pain Research, 21, 133-139 (2006)   2006.8

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  • 神経因性疼痛におけるミクログリア発現分子の役割

    津田誠,井上和秀

    日本神経精神薬理学雑誌 26, 57-61(2006)   2006.2

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  • 脊髄ミクログリア細胞の痛みへの役割

    津田誠,井上和秀

    Pain Research, 21, 1-4 (2006)   2006.2

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  • 神経因性疼痛とATP受容体

    井上和秀,津田誠

    日薬理誌, 127, 14-17 (2006)   2006.1

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  • ATP receptors in pain sensation: Involvement of spinal microglia and P2X4 receptors.

    Inoue K, Tsuda M, Koizumi S.

    Purinergic Signalling, 1, 95-100 (2005).   2005.4

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  • ATP- and adenosine-mediated signaling in the central nervous system: chronic pain and microglia: involvement of the ATP receptor P2X4.

    Inoue K, Tsuda M, Koizumi S.

    J Pharmacol Sci. 2004 Feb;94(2):112-4.   2004.2

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  • The functions of ATP receptors in the synaptic transmission in the hippocampus.

    Inoue K, Koizumi S, Ueno S, Kita A, Tsuda M.

    Prog Brain Res. 1999;120:193-206.   1999.11

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  • Contribution of glutamate receptors to benzodiazepine withdrawal signs.

    Tsuda M, Shimizu N, Suzuki T.

    Jpn J Pharmacol. 1999 Sep;81(1):1-6.   1999.9

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Industrial property rights

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Professional Memberships

  • 日本薬学会

  • Society for Neuroscience

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  • THE JAPANESE BIOCHEMICAL SOCIETY

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  • JAPANESE ASSOCIATION FOR THE STUDY OF PAIN

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  • THE JAPANESE SOCIETY FOR NEUROCHEMISTRY

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  • THE JAPAN NEUROSCIENCE SOCIETY

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  • THE JAPANESE SOCIETY OF NEUROPSYCHOPHARMACOLOGY

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  • THE JAPANESE PHARMACOLOGICAL SOCIETY

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  • 日本運動器疼痛研究会

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Committee Memberships

  • 日本神経精神薬理学会   企画・研究委員会委員   Domestic

    2025.2   

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    Committee type:Academic society

  • 日本薬理学会   百周年準備委員会   Domestic

    2024.4   

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    Committee type:Academic society

  • 日本神経化学会   優秀賞・奨励賞選考委員会 委員長  

    2023.9   

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    Committee type:Academic society

  • 日本神経化学会   Executive   Domestic

    2023.3   

  • 日本神経化学会   脳研究推進委員会委員  

    2021.6   

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    Committee type:Academic society

  • 日本薬理学会   Executive   Domestic

    2020.4 - 2024.3   

  • 日本運動器疼痛研究会   Steering committee member   Domestic

    2018.4 - Present   

  • 日本運動器疼痛研究会   編集委員会委員   Domestic

    2018.4 - Present   

  • 日本薬理学会   Steering committee member   Domestic

    2018.4 - 2020.3   

  • 日本薬理学会   財務委員   Domestic

    2018.4 - 2020.3   

  • 日本神経化学会   Steering committee member   Domestic

    2017.9 - 2021.3   

  • 日本神経化学会   優秀賞・奨励賞選考委員会委員   Domestic

    2017.9 - 2021.3   

  • 日本神経精神薬理学会   Steering committee member   Domestic

    2016.10 - 2018.10   

  • 日本神経精神薬理学会   先端研究推進基盤構築タスクフォース委員   Domestic

    2016.10 - 2018.10   

  • 日本薬理学会   Steering committee member   Domestic

    2016.4 - 2018.3   

  • 日本薬理学会   Steering committee member   Domestic

    2016.4 - 2018.3   

  • 日本薬理学会   編集委員会委員   Domestic

    2016.4 - 2018.3   

  • 日本薬理学会   賞等選考委員会委員   Domestic

    2016.4 - 2018.3   

  • 日本疼痛学会   Executive   Domestic

    2014.6   

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    Committee type:Academic society

  • 日本神経精神薬理学会   Councilor   Domestic

    2012.10 - Present   

  • 日本薬理学会   代議員   Domestic

    2012.4 - 2013.3   

  • 日本疼痛学会   Councilor   Domestic

    2010.7 - Present   

  • 日本運動器疼痛学会   Councilor   Domestic

    2008.12 - Present   

  • 日本神経化学会   Councilor   Domestic

    2008.9 - Present   

  • 日本薬理学会   代議員   Domestic

    2006.10 - 2008.9   

  • 日本薬理学会   Councilor   Domestic

    2005.4 - Present   

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Academic Activities

  • 第48回日本生物学的精神医学会年会・第36回日本臨床精神神経薬理学会年会・第56回日本神経精神薬理学会年会・第10回日本精神薬学会総会・学術集会合同年会(BCNP2026) プログラム委員

    Role(s): Planning, management, etc., Peer review

    2026.10 - 2026.11

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    Type:Academic society, research group, etc. 

  • 第68回日本神経化学会大会 プログラム委員

    第68回日本神経化学会大会  ( Japan ) 2025.9

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    Type:Competition, symposium, etc. 

  • 日本薬学会第145年会 シンポジウム オーガナイザー・座長

    Role(s): Planning, management, etc., Panel moderator, session chair, etc.

    2025.3

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    Type:Academic society, research group, etc. 

  • 第98回日本薬理学会・第102回日本生理学会・第130回日本解剖学会 合同大会 シンポジウムオーガナイザー・座長

    Role(s): Planning, management, etc., Panel moderator, session chair, etc.

    2025.3

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    Type:Academic society, research group, etc. 

  • 第46回日本疼痛学会 シンポジウム オーガナイザー・座長

    Role(s): Planning, management, etc., Panel moderator, session chair, etc.

    2024.11

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    Type:Academic society, research group, etc. 

  • グリアデコード国際シンポジウム オーガナイザー International contribution

    Role(s): Planning, management, etc., Panel moderator, session chair, etc.

    2024.7

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    Type:Competition, symposium, etc. 

  • NEURO2024 実行委員長,プログラム委員

    NEURO2024  ( Japan ) 2024.7

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    Type:Competition, symposium, etc. 

  • 第51回日本毒性学会学術年会 シンポジウム オーガナイザー・座長

    Role(s): Planning, management, etc., Panel moderator, session chair, etc.

    2024.7

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    Type:Academic society, research group, etc. 

  • 第51回日本毒性学会学術年会 企画委員

    第51回日本毒性学会学術年会  ( Japan ) 2024.7

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    Type:Academic society, research group, etc. 

  • Peer review of academic papers International contribution

    Role(s): Peer review

    2024.4 - 2025.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:32

    Proceedings of domestic conference Number of peer-reviewed papers:34

  • プログラム委員

    第96回日本生化学会大会  ( Japan ) 2023.10 - 2023.11

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第46回日本神経科学大会  ( Japan ) 2023.8

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    Type:Competition, symposium, etc. 

  • Peer review of academic papers

    Role(s): Peer review

    2023.4 - 2024.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:16

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:38

  • Pain Research International contribution

    2023.4 - Present

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    Type:Academic society, research group, etc. 

  • 特別講演座長

    日本薬学会第143年会  ( Japan ) 2023.3

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    Type:Competition, symposium, etc. 

  • シンポジウム座長

    日本生理学会第100回記念大会  ( Japan ) 2023.3

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    Type:Competition, symposium, etc. 

  • 一般演題座長

    第44回日本疼痛学会  ( Japan ) 2022.12

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第96回日本薬理学会年会  ( Japan ) 2022.11 - 2022.12

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    Type:Competition, symposium, etc. 

  • ポスター演題座長

    第96回日本薬理学会年会  ( Japan ) 2022.11 - 2022.12

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    Type:Competition, symposium, etc. 

  • 一般演題座長

    第75回日本薬理学会西南部会  ( Japan ) 2022.10

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    Type:Competition, symposium, etc. 

  • プログラム委員

    NEURO2022(第45 回日本神経科学大会・第65 回日本神経化学会大会・第32 回日本神経回路学会大会)  ( Japan ) 2022.6 - 2022.7

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    Type:Competition, symposium, etc. 

  • 一般演題座長

    Neuro2022  ( Japan ) 2022.5 - 2022.6

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    Type:Competition, symposium, etc. 

  • 特別企画シンポジウム座長

    第15回日本緩和医療薬学会年会  ( Japan ) 2022.5

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    Type:Competition, symposium, etc. 

  • Peer review of academic papers

    Role(s): Peer review

    2022.4 - 2023.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:23

    Number of peer-reviewed articles in Japanese journals:1

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:27

  • AMED-CREST, PRIME「老化」領域 アドバイザー

    Role(s): Review, evaluation

    AMED  2022.4 - Present

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    Type:Scientific advice/Review 

  • シンポジウムオーガナイザー&座長

    第95回日本薬理学会年会  ( Japan ) 2022.3

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    Type:Competition, symposium, etc. 

  • 組織委員

    第95回日本薬理学会年会  ( Japan ) 2022.3

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    Type:Competition, symposium, etc. 

  • 組織委員

    第95回日本薬理学会年会  ( Japan ) 2022.3

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    Type:Competition, symposium, etc. 

  • 一般演題座長

    第43回日本疼痛学会  ( Japan ) 2021.12

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー&座長

    第43回日本疼痛学会  ( Japan ) 2021.11

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー&座長

    第94回日本生化学会  ( Japan ) 2021.11

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    Type:Competition, symposium, etc. 

  • 主催

    第5回感覚フロンティア研究会シンポジウム  ( Japan ) 2021.10

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    Type:Competition, symposium, etc. 

  • Peer review of academic papers

    Role(s): Peer review

    2021.4 - 2022.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:30

    Number of peer-reviewed articles in Japanese journals:1

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:37

  • シンポジウムオーガナイザー&座長

    第126回日本解剖学会総会・全国学術集会・第98回日本生理学会大会  ( Japan ) 2021.3

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第42回日本疼痛学会  ( Japan ) 2020.12

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    Type:Competition, symposium, etc. 

  • Frontiers in Pain Research International contribution

    2020.10 - Present

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    Type:Academic society, research group, etc. 

  • Frontiers in Molecular Neuroscience International contribution

    2020.6 - Present

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    Type:Academic society, research group, etc. 

  • プログラム委員

    第14回日本緩和医療薬学会年会  ( Japan ) 2020.5

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    Type:Competition, symposium, etc. 

  • AMED-CREST, PRIME「適応・修復」領域 科学技術調査員(外部査読委員)

    Role(s): Review, evaluation

    AMED  2020.5 - 2020.7

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    Type:Scientific advice/Review 

  • Peer review of academic papers

    Role(s): Peer review

    2020.4 - 2021.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:49

    Number of peer-reviewed articles in Japanese journals:2

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:8

  • プログラム委員

    第93回日本薬理学会年会  ( Japan ) 2020.3

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    Type:Competition, symposium, etc. 

  • Neuroscience Research International contribution

    2020.1 - 2022.12

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    Type:Academic society, research group, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2019.12 - 2020.11

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    Type:Scientific advice/Review 

  • プログラム委員

    第6回アジア神経精神薬理学会大会(AsCNP2019)  ( Japan ) 2019.10

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    Type:Competition, symposium, etc. 

  • Organizing Committee

    第48回内藤コンファレンス  ( Japan ) 2019.10

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    Type:Competition, symposium, etc. 

    Number of participants:100

  • プログラム委員

    第42回日本神経科学大会・第62回日本神経化学会大会合同大会(Neuro2019)  ( Japan ) 2019.7

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    Type:Competition, symposium, etc. 

  • プログラム・査読委員

    第41回日本疼痛学会  ( Japan ) 2019.7

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第13回日本緩和医療薬学会年会  ( Japan ) 2019.5 - 2019.6

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    Type:Competition, symposium, etc. 

  • AMED-CREST, PRIME「適応・修復」領域 科学技術調査員(外部査読委員)

    Role(s): Review, evaluation

    AMED  2019.5 - 2019.7

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    Type:Scientific advice/Review 

  • Peer review of academic papers

    Role(s): Peer review

    2019.4 - 2020.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:32

    Number of peer-reviewed articles in Japanese journals:1

    Proceedings of International Conference Number of peer-reviewed papers:27

    Proceedings of domestic conference Number of peer-reviewed papers:10

  • シンポジウムオーガナイザー

    日本薬学会第139年会  ( Japan ) 2019.3

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    第92回日本薬理学会年会  ( Japan ) 2019.3

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    Type:Competition, symposium, etc. 

  • 一般演題座長

    第11回日本運動器疼痛学会  ( Japan ) 2018.12

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    Type:Competition, symposium, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2018.12 - 2019.11

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    Type:Scientific advice/Review 

  • 一般演題座長

    第71回日本薬理学会西南部会  ( Japan ) 2018.11

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    Type:Competition, symposium, etc. 

  • 実行委員

    第71回日本薬理学会西南部会  ( Japan ) 2018.11

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    Type:Competition, symposium, etc. 

  • カナダNSERCグラント審査員

    Role(s): Review, evaluation

    カナダNSERC  2018.11

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    Type:Scientific advice/Review 

  • シンポジウムオーガナイザー

    第61回日本神経化学会  ( Japan ) 2018.9

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    生体機能と創薬シンポジウム2018  ( Japan ) 2018.8

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    Type:Competition, symposium, etc. 

  • Oral session座長 International contribution

    18th World Congress of Basic and Clinical Pharmacology (WCP2018)  ( Japan ) 2018.7

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    Type:Competition, symposium, etc. 

  • 教育講演座長

    第40回日本疼痛学会  ( Japan ) 2018.6

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第40回日本疼痛学会  ( Japan ) 2018.6

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    Type:Competition, symposium, etc. 

  • AMED-CREST, PRIME「適応・修復」領域 科学技術調査員(外部査読委員)

    Role(s): Review, evaluation

    AMED  2018.5 - 2018.8

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    Type:Scientific advice/Review 

  • Peer review of academic papers

    Role(s): Peer review

    2018.4 - 2019.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:33

    Number of peer-reviewed articles in Japanese journals:2

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:53

  • Neuroscience Bulletin International contribution

    2018.1 - 2020.12

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    Type:Academic society, research group, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2017.12 - 2018.11

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    Type:Scientific advice/Review 

  • 公益財団法人 国際科学技術財団 研究助成選考委員

    Role(s): Review, evaluation

    公益財団法人 国際科学技術財団  2017.12 - 2018.4

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    Type:Scientific advice/Review 

  • 座長

    第10回日本運動器疼痛学会  ( Japan ) 2017.11

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    Type:Competition, symposium, etc. 

  • カナダNSERCグラント審査員

    Role(s): Review, evaluation

    NSERC  2017.11 - 2018.1

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    Type:Scientific advice/Review 

  • プログラム委員

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会 合同年会  ( Japan ) 2017.9

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会 合同年会  ( Japan ) 2017.9

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第60回神経化学会大会  ( Japan ) 2017.9

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第60回神経化学会大会  ( Japan ) 2017.9

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    Type:Competition, symposium, etc. 

  • 座長

    第60回神経化学会大会  ( Japan ) 2017.9

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    Type:Competition, symposium, etc. 

  • 実行委員

    生体機能と創薬シンポジウム2017  ( Japan ) 2017.8

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    生体機能と創薬シンポジウム2017  ( Japan ) 2017.7

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    Type:Competition, symposium, etc. 

  • Peer review of academic papers

    Role(s): Peer review

    2017.4 - 2018.3

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:43

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:17

  • 国際事業委員会書面評価委員

    Role(s): Review, evaluation

    日本学術振興会  2017.4 - 2018.3

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    Type:Scientific advice/Review 

  • 組織委員

    第90回日本薬理学会年会  ( Japan ) 2017.3

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    Type:Competition, symposium, etc. 

  • 組織委員

    第90回日本薬理学会年会  ( Japan ) 2017.3

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    第90回日本薬理学会年会  ( Japan ) 2017.3

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    Type:Competition, symposium, etc. 

  • シンポジウムコメンテーター

    第90回日本薬理学会年会  ( Japan ) 2017.3

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    Type:Competition, symposium, etc. 

  • 主催

    平成28年度 岡崎生理研研究会「痛みの理解を目指した先端的アプローチ」  ( Japan ) 2017.1

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    Type:Competition, symposium, etc. 

    Number of participants:100

  • 主催

    平成28年度 岡崎生理研研究会  ( Japan ) 2017.1

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第69回日本薬理学会西南部会  ( Japan ) 2016.11

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    Type:Competition, symposium, etc. 

  • 大学設置・学校法人審議会(大学設置分科会)専門委員

    Role(s): Review, evaluation

    文部科学省  2016.11 - 2017.10

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    Type:Scientific advice/Review 

  • 座長(Chairmanship)

    第60回日本神経化学会大会  ( Japan ) 2016.9

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    Type:Competition, symposium, etc. 

  • プログラム委員

    第46回日本神経精神薬理学会  ( SouthKorea ) 2016.7

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第38回日本疼痛学会  ( Japan ) 2016.6 - 2016.4

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    Type:Competition, symposium, etc. 

  • J Pharmacol Sci International contribution

    2016.4 - 2018.3

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    Type:Academic society, research group, etc. 

  • 座長(Chairmanship)

    第89回日本薬理学会年会  ( Japan ) 2016.3

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    Type:Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    第89回日本薬理学会年会  ( Japan ) 2016.3

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    Type:Competition, symposium, etc. 

  • 主催

    平成27年度 岡崎生理研研究会「痛みの理解を目指した先端的アプローチ」  ( Japan ) 2015.12

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    Type:Competition, symposium, etc. 

    Number of participants:100

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2015.12 - 2016.11

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    Type:Scientific advice/Review 

  • プログラム委員

    第45回日本神経精神薬理学会  ( Japan ) 2015.9

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第58回神経化学会大会  ( Japan ) 2015.9 - 2016.9

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第38回日本神経科学大会  ( Japan ) 2015.7

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    日本薬学会第135年会  ( Japan ) 2015.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第31回日本薬学会九州支部大会  ( Japan ) 2014.12

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    Type:Competition, symposium, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2014.12 - 2015.11

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    Type:Scientific advice/Review 

  • 座長(Chairmanship)

    第67回日本薬理学会西南部会  ( Japan ) 2014.11

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    Type:Competition, symposium, etc. 

  • グラント審査委員

    Role(s): Review, evaluation

    UAE University  2014.11 - 2015.11

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    Type:Scientific advice/Review 

  • プログラム委員

    第8回日本緩和医療薬学会年会  ( Japan ) 2014.10

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第130回日本薬理学会関東部会  ( Japan ) 2014.7

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship) International contribution

    日本学術振興会二国間(日独)交流事業研究セミナー  ( Germany ) 2014.6 - 2014.7

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    Type:Competition, symposium, etc. 

  • オーガナイザー

    日本薬学会第134年会  ( Japan ) 2014.3

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    Type:Competition, symposium, etc. 

  • オーガナイザー

    第87回日本薬理学会年会  ( Japan ) 2014.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship) International contribution

    Areces Foundation Symposium  ( Madrid Spain ) 2014.3

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    Type:Competition, symposium, etc. 

  • 主催

    第4回福岡薬理・生理研究会  ( Japan ) 2013.12

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第66回日本薬理学会西南部会  ( Japan ) 2013.11

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    Type:Competition, symposium, etc. 

  • 実行委員

    生体機能と創薬シンポジウム  ( Japan ) 2013.8

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    Type:Competition, symposium, etc. 

  • プログラム委員

    Neuro2013  ( Japan ) 2013.6 - 2014.6

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    Neuro2013  ( Japan ) 2013.6

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第86回日本薬理学会年会  ( Japan ) 2013.3

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    Type:Competition, symposium, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2012.12 - 2013.11

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    Type:Scientific advice/Review 

  • 座長(Chairmanship)

    第5回運動器疼痛学会  ( Japan ) 2012.11

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第11回次世代を担う若手ファーマバイオフォーラム  ( Japan ) 2012.9

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    Type:Competition, symposium, etc. 

  • 不明

    日本麻酔科学会第59回学術集会  ( Japan ) 2012.6

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    Type:Competition, symposium, etc. 

  • 事務局長 International contribution

    Purine2012  ( Fukuoka Japan ) 2012.5 - 2012.6

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    Type:Competition, symposium, etc. 

    Number of participants:330

  • カナダNSERCグラント審査員

    Role(s): Review, evaluation

    NSERC  2011.11 - 2012.1

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    Type:Scientific advice/Review 

  • 座長(Chairmanship)

    第84回日本薬理学会年会  ( Japan ) 2011.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第85回日本薬理学会年会  ( Japan ) 2011.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第21回神経行動薬理若手研究者の集い  ( Japan ) 2011.3

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    Type:Competition, symposium, etc. 

  • 科学研究費委員会専門委員

    Role(s): Review, evaluation

    日本学術振興会  2010.11

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    Type:Scientific advice/Review 

  • 実行委員

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  ( Japan ) 2010.9

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    Type:Competition, symposium, etc. 

    Number of participants:4,000

  • 座長(Chairmanship)

    Neuro2010(第33回日本神経科学大会、第53回日本神経化学会大会ならびに第20回日本神経回路学会大会)  ( Japan ) 2010.9

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第83回日本薬理学会年会  ( Japan ) 2010.3

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    Type:Competition, symposium, etc. 

  • 科学研究費委員会・専門委員

    Role(s): Review, evaluation

    日本学術振興会  2009.11

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    Type:Scientific advice/Review 

  • 実行委員 International contribution

    Fukuoka Purine 2009  ( Japan ) 2009.7 - 2010.7

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    Type:Competition, symposium, etc. 

    Number of participants:200

  • 座長(Chairmanship)

    第18回神経行動薬理若手研究者の集い  ( Japan ) 2009.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第82回日本薬理学会年会  ( Japan ) 2009.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    トランスポーターワークショップ IN 福岡  ( Japan ) 2008.11

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    生理学研究所研究会『病態と細胞外プリン-治療標的としての可能性を探る』  ( Japan ) 2008.9

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    Type:Competition, symposium, etc. 

  • 第30回日本疼痛学会 / 福岡ペイン2008 プログラム委員

    第30回日本疼痛学会 / 福岡ペイン2008  ( Japan ) 2008.7

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    Type:Competition, symposium, etc. 

    Number of participants:2,500

  • 座長(Chairmanship)

    第80回日本薬理学会年会  ( Japan ) 2007.3

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    平成18年度生理研研究会「痛みの分子メカニズムと治療戦略」  ( Japan ) 2006.11

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    平成18年度生理学研究所研究会「Neuro-glio-vascular interaction におけるプリン作動性シグナリングの病態生理的機能」  ( Japan ) 2006.9

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship)

    第40回日本ペインクリニック学会  ( Japan ) 2006.7

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    Type:Competition, symposium, etc. 

  • 座長(Chairmanship) International contribution

    The fifth Japan-Korea Joint Symposium of Brain Sciences, and Cardiac and Smooth Muscles  ( Japan ) 2005.7

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    Type:Competition, symposium, etc. 

▼display all

Other

  • 神経障害性疼痛とミクログリアに関する総説「Microglial diversity in neuropathic pain」がTrends in Neuroscience誌(IF:14.6)に掲載された

    2023.6

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    神経障害性疼痛とミクログリアに関する総説「Microglial diversity in neuropathic pain」がTrends in Neuroscience誌に掲載された。

  • 学術論文「Neuronal pentraxin 2 is required for facilitating excitatory synaptic inputs onto spinal neurons involved in pruriceptive transmission in a model of chronic itch」がNature Commun誌(IF:17.694)に掲載された。

    2022.5

  • 学術論文「A spinal microglia population involved in remitting and relapsing neuropathic pain」がScience誌(IF:47.728)に掲載された。

    2022.4

  • 学術論文「Astrocytic STAT3 activation and chronic itch require IP3R1/TRPC-dependent Ca2+ signals in mice」がJ Allergy Clin Immunol 誌(IF:10.793)に掲載された。

    2021.4

  • 学術論文「A subset of spinal dorsal horn interneurons crucial for gating touch-evoked pain-like behavior」がPNAS誌(IF:11.205)に掲載された。

    2021.1

  • 学術論文「Spinal astrocytes in superficial laminae gate brainstem descending control of mechanosensory hypersensitivity」がNature Neuroscience誌(IF:20.071)に掲載された。

    2020.10

  • 学術論文「Sensitization of spinal itch transmission neurons in a mouse model of chronic itch requires an astrocytic factor」がJ Allergy Clin Immunol 誌(IF:14.11)に掲載された。

    2020.1

  • 学術論文「Role of P2X3 receptors in scratching behavior in mouse models」がJ Allergy Clin Immunol 誌に掲載された。

    2019.1

  • 神経障害性疼痛とミクログリアに関する総説「Microglia in neuropathic pain: cellular and molecular mechanisms and therapeutic potential」がNature Reviews Neuroscience誌に掲載された。

    2018.3

  • 学術論文「STAT3-dependent reactive astrogliosis in the spinal dorsal horn underlies chronic itch」がNature Medicine誌に掲載された。

    2015.7

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Research Projects

  • Elucidation of the mechanism for biological resilience to neuropathic pain and their application to diagnosis and treatment

    Grant number:24H00067  2024 - 2028

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (S)

    津田 誠, 藤井 敬之

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    Authorship:Principal investigator  Grant type:Scientific research funding

    神経系の障害により発症する神経障害性疼痛には有効な治療法がないため、その克服に向けた疼痛の慢性化機序の解明が求められている。代表者は最近、神経障害性疼痛モデルマウスの脊髄において痛みの慢性化を抑止する細胞(CD11c陽性ミクログリア)を発見した。本研究では、同細胞の誘導・機能獲得・神経制御機構を解明し、さらに慢性疼痛との関連性をヒトで検証することで、神経障害性疼痛に対する生体レジリエンス機構を明らかにし、新たな診断・治療法の開発に向けた基盤の構築を目指す。

    CiNii Research

  • 生体ストレスによる痛み発生・変調機構の解明と慢性疼痛診断治療技術の開発

    2023 - 2028

    AMED  AMED-CREST  AMED-CREST

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    Authorship:Principal investigator  Grant type:Contract research

  • Glia decoding: deciphering information critical for brain-body interactions

    Grant number:20H05894  2020.11 - 2025.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Transformative Research Areas (A)

    岡部 繁男, 星野 歩子, 松田 道行, 小泉 修一, 石井 優, 田中 謙二, 津田 誠, 史 蕭逸, 小山 隆太, 和氣 弘明

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    Grant type:Scientific research funding

    脳の広範な機能の理解には神経細胞以外の細胞要素、特に神経細胞と接して存在するグリア細胞の情報を読み出す必要がある。本領域の目標はグリア細胞の状態・機能・細胞間シグナル伝達を包括的に読み出す技術(デコーディング技術)を開発し、脳と身体の間での生体情報の統合を理解する所にある。このような研究を推進するには従来の脳科学研究の成果を踏まえつつも、全く異なるアイディアや計測技術を取り込み、異分野との連携を行う必要がある。総括班ではこのような研究の新規性、技術的優位性、異分野連携に特に力を入れて目標達成に向けた領域の推進に貢献する。

    CiNii Research

  • Modification of somatosensory behaviors by intervention of glial cell subsets

    Grant number:20H05900  2020.11 - 2025.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Transformative Research Areas (A)

    津田 誠, 齊藤 秀俊

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    Grant type:Scientific research funding

    本研究では,脊髄でのグリア細胞の多様性と,体性感覚(特に痛みと痒み)の情報処理とその結果として表出する行動におけるサブセット独自の役割を明らかにする。さらに,脳からのトップダウンシグナルや末梢組織からの遠隔シグナルなどに注目し,グリアサブセットの活動制御メカニズムも明らかにする。また,慢性的な痛みや痒みにおけるグリアサブセットの役割も明らかにし,その治療応用に向けた基盤技術の創出を目指す。

    CiNii Research

  • Elucidation of abnormal functioning of neuronal circuits underlying neuropathic pain and its application for drug discovery

    Grant number:19H05658  2019 - 2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (S)

    Tsuda Makoto

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    Authorship:Principal investigator  Grant type:Scientific research funding

    Combining our newly established method for evaluating neuropathic allodynia by selective stimulation of primary afferent Aβ fibers (touch-sensing fibers) with a method for regulating cell subset-specific functions using viral vectors, we identified several neuronal and glial subsets important for neuropathic allodynia. In particular, dysfunction of the NPY+ neuronal subset after nerve injury was found to play a central role in the development of neuropathic allodynia. In addition, we found that signaling from glial cells is responsible for the dysfunction of NPY+ neurons. Furthermore, we also showed that an analgesic effect of the clinically approved drug duloxetine requires the activation of NPY+ neurons, and we identified compounds that can enhance the function of NPY+ neurons.

    CiNii Research

  • 神経障害性アロディニアに直結する神経回路機能異常の解明(*基盤S採択のため中止)

    Grant number:19H01059  2019 - 2022

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 痒みの情報伝達における新しい脊髄後角神経回路の特定

    Grant number:19K22500  2019 - 2020

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Challenging Research(Exploratory)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • メカノ作動性分子を標的としたドラッグリポジショニング研究

    2018.4 - 2019.4

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • 第47回内藤記念特定研究助成金

    2018

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    Grant type:Donation

  • メカノ作動性分子を標的としたドラッグリポジショニング研究

    2017.4 - 2018.3

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • ATP受容体によるインスリン開口分泌調整機構の解明

    2017.4 - 2018.3

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • 慢性の痒みと痛みのメカニズムと治療法の開発に関する研究

    2016.6 - 2018.3

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • メカノ作動性分子を標的としたドラッグリポジショニング研究

    2016.4 - 2017.3

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • 慢性疼痛における糖脂質シグナルの作動機序解明と創薬に向けた研究

    2016 - 2020

    AMED 革新的先端研究開発支援事業

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    Authorship:Coinvestigator(s)  Grant type:Contract research

  • 皮膚バリアに影響する一次求心性神経由来シグナル分子の特定

    2016 - 2018

    AMED 免疫アレルギー疾患等実用化研究事業(免疫アレルギー疾患実用化研究分野)

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    Authorship:Principal investigator  Grant type:Contract research

  • 慢性掻痒に重要な脊髄アストロサイトの活性化に関与する一次求心性神経の特定

    2016 - 2017

    Japan Society for the Promotion of Science  Bilateral program

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    Authorship:Principal investigator  Grant type:Joint research

  • 新しいミクログリア細胞群を切り口とした神経障害性疼痛の慢性化メカニズムの解明

    Grant number:15H02522  2015 - 2018

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • アトピー性皮膚炎の慢性掻痒メカニズムの解明を目指した新しい研究アプローチ

    Grant number:15K15203  2015 - 2016

    Grants-in-Aid for Scientific Research  Grant-in-Aid for challenging Exploratory Research

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 難治性慢性疼痛の神経科学的メカニズムの解明

    2014.4 - 2015.3

    Joint research

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    Authorship:Principal investigator  Grant type:Other funds from industry-academia collaboration

  • JSPS日独二国間交流セミナー International coauthorship

    2014.4 - 2015.3

    日本 

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    Authorship:Coinvestigator(s) 

  • 脳内ミクログリアによるシナプス制御機構と慢性疼痛

    2014 - 2017

    Japan Society for the Promotion of Science・Ministry of Education, Culture, Sports, Science and Technology  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research on Innovative Areas

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 慢性疼痛のトランスレーショナルリサーチ:精神心理学的・神経免疫学的側面からの病態解明と評価法開発

    2014 - 2015

    Grants-in-Aid for Scientific Research  Grants-in-Aid for Scientific Research (Ministry of Health, Labour and Welfare)

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    Authorship:Coinvestigator(s)  Grant type:Competitive funding other than Grants-in-Aid for Scientific Research

  • Progress100

    2014 - 2015

    平成26年度運営費交付金特別経費(国立大学の機能強化)による世界トップレベル研究者招へいプログラム「Progress 100」

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    Authorship:Principal investigator  Grant type:On-campus funds, funds, etc.

  • 武田科学振興財団ビジョナリーリサーチ助成

    2014

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    Grant type:Donation

  • アステラス病態代謝研究会研究助成金

    2014

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    Grant type:Donation

  • 東レ科学技術研究助成

    2014

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    Grant type:Donation

  • 炎症の慢性化機構の解明と制御に向けた基盤技術の創出

    2011 - 2015

    JST Strategic Basic Research Program (Ministry of Education, Culture, Sports, Science and Technology)

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    Authorship:Collaborating Investigator(s) (not designated on Grant-in-Aid)  Grant type:Contract research

  • ミクログリア転写因子IRF8を介する神経障害性疼痛発症維持メカニズム(*内閣府NEXTの採択に伴う重複制限で辞退)

    Grant number:23249031  2011 - 2014

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 情動的側面に着目した慢性疼痛の病態解明と診断・評価法の開発

    2011 - 2013

    Grants-in-Aid for Scientific Research  Grants-in-Aid for Scientific Research (Ministry of Health, Labour and Welfare)

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    Authorship:Collaborating Investigator(s) (not designated on Grant-in-Aid)  Grant type:Competitive funding other than Grants-in-Aid for Scientific Research

  • ミクログリア転写因子IRF8を切り口にした慢性疼痛メカニズムの解明

    2010 - 2013

    Japan Society for the Promotion of Science  最先端・次世代研究開発支援プログラム

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    Authorship:Principal investigator  Grant type:Joint research

  • 活性化ミクログリアによるニューロンネットワーク機能変調の機構解明

    2009 - 2014

    JST Strategic Basic Research Program (Ministry of Education, Culture, Sports, Science and Technology)

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    Authorship:Principal investigator  Grant type:Contract research

  • グリアーニューロン相互作用をターゲットとした難治性疼痛発症機序解明と創薬への展開

    2009 - 2010

    Japan Society for the Promotion of Science  先端研究拠点事業 拠点形成型

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    Authorship:Coinvestigator(s)  Grant type:Joint research

  • 神経損傷によるミクログリア細胞増殖とその神経因性疼痛発症における役割

    2009

    持田記念医学薬学新興財団 研究助成金

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    Authorship:Principal investigator  Grant type:Contract research

  • ミクログリアにおけるATP受容体の発現を誘導するニューロン由来疼痛関連因子

    2009

    病態代謝研究会

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    Authorship:Principal investigator  Grant type:Contract research

  • ミクログリア細胞においてP2X4受容体依存的に誘導される神経因性疼痛遺伝子の特定

    Grant number:20689030  2008 - 2010

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (A)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 第40回病態代謝研究会研究助成金/ミクログリアにおけるATP受容体の発現を誘導するニューロン由来疼痛関連因子

    2008

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    Grant type:Donation

  • 第26回持田記念研究助成金/神経損傷によるミクログリア細胞増殖とその神経因性疼痛発症における役割

    2008

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    Grant type:Donation

  • -

    2007 - 2009

    総長裁量経費にかかる研究スーパースター支援プログラム

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    Authorship:Principal investigator  Grant type:On-campus funds, funds, etc.

  • 神経因性疼痛発症メカニズムの解明

    2006 - 2010

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Creative Scientific Research

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 細胞外ATPを介したアストログリアーニュロン相互調節機構の解明

    2005 - 2007

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research on Priority Areas

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    Authorship:Coinvestigator(s)  Grant type:Scientific research funding

  • 難治性疼痛におけるグリア細胞活性化の分子的基盤

    Grant number:17689042  2005 - 2007

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (A)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 難治性慢性疼痛時のミクログリアにおけるP2X4受容体発現増強分子の同定

    Grant number:17650111  2005 - 2006

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Exploratory Research

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • ミクログリア由来疼痛関連液性因子の同定

    2005

    武田科学振興財団・薬学系研究奨励

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    Authorship:Principal investigator  Grant type:Contract research

  • 難治性疼痛時の脊髄ミクログリアにおけるP2X4受容体発現増強機構の解明

    2005

    上原記念生命科学財団・研究奨励金

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    Authorship:Principal investigator  Grant type:Contract research

  • 2005年度薬学系研究奨励金 / ミクログリア由来疼痛関連液性因子の同定

    2005

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    Grant type:Donation

  • 日本ーカナダ2国間医学研究協力事業 International coauthorship

    2004.4 - 2006.3

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    Authorship:Coinvestigator(s) 

    P2X4による疼痛発現メカニズムを明らかにする

  • 難治性疼痛におけるグリア由来因子の役割

    2002

    上原記念生命科学財団・ポストドクトラルフェローシップ

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    Authorship:Principal investigator  Grant type:Contract research

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Educational Activities

  • 薬理学II(2年冬期): 神経系疾患の病態機序,症状,治療薬の薬理作用について講義する。
    薬学少人数ゼミナール: 研究内容を紹介する。
    創薬科学総論(1年): 痛みと痒みに関する神経科学的メカニズムを学習する。
    先端研究実験I(大学院): 所属分野の研究内容に即した最新科学実験技術を指導する。論文を読み,それについてディスカッションする。
    先端研究実験II(大学院): 先端研究実験Iで習得した様々な研究能力の向上を目指す。
    医療薬学演習I(大学院): 大学院生(修士1年生)の研究テーマについて発表させ,ディスカッションする。
    医療薬学演習II(大学院): 大学院生(修士2年生)の研究テーマについて発表させ,ディスカッションする。
    薬理・基礎理論(大学院): 薬理学・生理学の基礎理論を深く学習する。
    薬理・疾患治療(大学院): 各種病態発症メカニズムを深く学習し,新薬開発の可能性を追求する。
    科学論文発表(大学院): 所属分野の研究内容に即した最新科学論文を読み,それについてディスカッションする。
    生体情報機能学Ⅱ(医学部): 痛みの仕組みとその慢性化メカニズム

Class subject

  • 卒業発表

    2024.10 - 2025.3   Second semester

  • 薬理・基礎理論

    2024.10 - 2025.3   Second semester

  • 生体情報機能学II

    2024.10 - 2025.3   Second semester

  • 卒業演習 中間演習

    2024.10 - 2025.3   Second semester

  • 薬理学Ⅱ

    2024.10 - 2025.2   Winter quarter

  • 薬学少人数ゼミナール

    2024.6 - 2025.9   Summer quarter

  • 創薬科学総論

    2024.4 - 2025.3   Full year

  • 薬学特別実習

    2024.4 - 2025.3   Full year

  • 卒業研究

    2024.4 - 2025.3   Full year

  • 先端研究実験I/II

    2024.4 - 2025.3   Full year

  • 医療薬学演習I/II

    2024.4 - 2025.3   Full year

  • 医療薬学系教育指導実習

    2024.4 - 2025.3   Full year

  • 薬学基礎実習IV

    2024.4 - 2024.8   First semester

  • 薬理学Ⅱ

    2023.12 - 2024.2   Winter quarter

  • 薬理・疾患治療

    2023.10 - 2024.3   Second semester

  • 創薬科学総論II/IV

    2023.4 - 2024.3   Full year

  • 薬理学Ⅱ

    2022.12 - 2023.2   Winter quarter

  • 薬理・基礎理論

    2022.10 - 2023.3   Second semester

  • 生体情報機能学Ⅱ

    2022.10 - 2023.3   Second semester

  • 薬学少人数ゼミナール

    2022.10 - 2023.3   Second semester

  • 薬理・基礎理論

    2022.10 - 2023.3   Second semester

  • 薬物治療学Ⅱ

    2022.6 - 2022.8   Summer quarter

  • 卒業実習(アドバンスト実務実習)

    2022.4 - 2023.3   Full year

  • 医療薬学系教育指導実習

    2022.4 - 2023.3   Full year

  • 科学論文発表

    2022.4 - 2023.3   Full year

  • 先端研究実験I/II

    2022.4 - 2023.3   Full year

  • 卒業研究 薬学特別実習

    2022.4 - 2023.3   Full year

  • 卒業研究

    2022.4 - 2023.3   Full year

  • 医療薬学演習I/II

    2022.4 - 2022.9   First semester

  • 医療薬学研究

    2022.4 - 2022.9   First semester

  • 薬理学Ⅱ

    2021.12 - 2022.2   Winter quarter

  • 薬理学Ⅱ

    2021.12 - 2022.2   Winter quarter

  • 薬理・疾患治療

    2021.10 - 2022.3   Second semester

  • 薬理・疾患治療

    2021.10 - 2022.3   Second semester

  • 薬学少人数ゼミナール

    2021.10 - 2022.3   Second semester

  • 生体情報機能学Ⅱ

    2021.10 - 2022.3   Second semester

  • 創薬科学総論III

    2021.10 - 2021.12   Fall quarter

  • 医療薬学系教育指導実習

    2021.4 - 2022.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2021.4 - 2022.3   Full year

  • 卒業研究

    2021.4 - 2022.3   Full year

  • 卒業研究 薬学特別実習

    2021.4 - 2022.3   Full year

  • 先端研究実験I

    2021.4 - 2022.3   Full year

  • 先端研究実験II

    2021.4 - 2022.3   Full year

  • 科学論文発表

    2021.4 - 2022.3   Full year

  • 医療薬学演習I

    2021.4 - 2021.9   First semester

  • 医療薬学演習II

    2021.4 - 2021.9   First semester

  • 医療薬学研究

    2021.4 - 2021.9   First semester

  • 薬理学Ⅱ

    2020.12 - 2021.2   Winter quarter

  • 生体情報機能学Ⅱ

    2020.10 - 2021.3   Second semester

  • 医療薬学系教育指導実習

    2020.10 - 2021.3   Second semester

  • 薬学少人数ゼミナール

    2020.10 - 2021.3   Second semester

  • 薬理・基礎理論

    2020.10 - 2021.3   Second semester

  • 創薬科学総論III

    2020.10 - 2020.12   Fall quarter

  • 先端研究実験I

    2020.4 - 2021.3   Full year

  • 科学論文発表

    2020.4 - 2021.3   Full year

  • 先端研究実験II

    2020.4 - 2021.3   Full year

  • 先端研究実験I

    2020.4 - 2021.3   Full year

  • 卒業研究 薬学特別実習

    2020.4 - 2021.3   Full year

  • 卒業研究

    2020.4 - 2021.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2020.4 - 2021.3   Full year

  • 医療薬学研究

    2020.4 - 2020.9   First semester

  • 医療薬学演習II

    2020.4 - 2020.9   First semester

  • 医療薬学演習I

    2020.4 - 2020.9   First semester

  • 薬理学Ⅱ

    2019.12 - 2020.2   Winter quarter

  • 薬理・疾患治療

    2019.10 - 2020.3   Second semester

  • 生体情報機能学Ⅱ

    2019.10 - 2020.3   Second semester

  • 医療薬学系教育指導実習

    2019.10 - 2020.3   Second semester

  • 薬学少人数ゼミナール

    2019.10 - 2020.3   Second semester

  • 創薬科学総論III

    2019.10 - 2019.12   Fall quarter

  • 科学論文発表

    2019.4 - 2020.3   Full year

  • 先端研究実験II

    2019.4 - 2020.3   Full year

  • 卒業研究 薬学特別実習

    2019.4 - 2020.3   Full year

  • 卒業研究

    2019.4 - 2020.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2019.4 - 2020.3   Full year

  • 医療薬学演習I

    2019.4 - 2019.9   First semester

  • 医療薬学研究

    2019.4 - 2019.9   First semester

  • 医療薬学演習II

    2019.4 - 2019.9   First semester

  • 薬理学Ⅱ

    2018.12 - 2019.2   Winter quarter

  • 薬理・基礎理論

    2018.10 - 2019.3   Second semester

  • 生体情報機能学Ⅱ

    2018.10 - 2019.3   Second semester

  • 医療薬学系教育指導実習

    2018.10 - 2019.3   Second semester

  • 薬学少人数ゼミナール

    2018.10 - 2019.3   Second semester

  • 創薬科学総論II

    2018.10 - 2019.3   Second semester

  • 卒業実習(アドバンスト実務実習)

    2018.4 - 2019.3   Full year

  • 科学論文発表

    2018.4 - 2019.3   Full year

  • 先端研究実験II

    2018.4 - 2019.3   Full year

  • 先端研究実験I

    2018.4 - 2019.3   Full year

  • 卒業研究 薬学特別実習

    2018.4 - 2019.3   Full year

  • 卒業研究

    2018.4 - 2019.3   Full year

  • 医療薬学演習I

    2018.4 - 2018.9   First semester

  • 医療薬学研究

    2018.4 - 2018.9   First semester

  • 医療薬学演習II

    2018.4 - 2018.9   First semester

  • 薬理学Ⅰ

    2017.12 - 2018.2   Winter quarter

  • 薬理・疾患治療

    2017.10 - 2018.3   Second semester

  • 生体情報機能学Ⅱ(医学部)

    2017.10 - 2018.3   Second semester

  • 医療薬学系教育指導実習

    2017.10 - 2018.3   Second semester

  • 薬学少人数ゼミナール

    2017.10 - 2018.3   Second semester

  • 創薬科学総論II

    2017.10 - 2018.3   Second semester

  • 卒業実習(アドバンスト実務実習)

    2017.4 - 2018.3   Full year

  • 科学論文発表

    2017.4 - 2018.3   Full year

  • 先端研究実験II

    2017.4 - 2018.3   Full year

  • 先端研究実験I

    2017.4 - 2018.3   Full year

  • 薬学特別実習

    2017.4 - 2018.3   Full year

  • 卒業研究

    2017.4 - 2018.3   Full year

  • 薬理・基礎理論

    2017.4 - 2017.9   First semester

  • 医療薬学研究

    2017.4 - 2017.9   First semester

  • 医療薬学演習II

    2017.4 - 2017.9   First semester

  • 医療薬学演習I

    2017.4 - 2017.9   First semester

  • 薬理学I

    2016.10 - 2017.3   Second semester

  • 生体情報機能学Ⅱ(医学部)

    2016.10 - 2017.3   Second semester

  • 医療薬学系教育指導実習

    2016.10 - 2017.3   Second semester

  • 医療薬学研究

    2016.10 - 2017.3   Second semester

  • 医療薬学演習I

    2016.10 - 2017.3   Second semester

  • 薬学少人数ゼミナール

    2016.10 - 2017.3   Second semester

  • 創薬科学総論II

    2016.10 - 2017.3   Second semester

  • 卒業実習(アドバンスト実務実習)

    2016.4 - 2017.3   Full year

  • 科学論文発表

    2016.4 - 2017.3   Full year

  • 先端研究実験II

    2016.4 - 2017.3   Full year

  • 先端研究実験I

    2016.4 - 2017.3   Full year

  • 薬学特別実習

    2016.4 - 2017.3   Full year

  • 卒業研究

    2016.4 - 2016.9   First semester

  • 医療薬学演習II

    2016.4 - 2016.9   First semester

  • 医療薬学系教育指導実習

    2015.10 - 2016.3   Second semester

  • 薬理・薬理疾患治療

    2015.10 - 2016.3   Second semester

  • 医療薬学研究

    2015.10 - 2016.3   Second semester

  • 薬学少人数ゼミナール

    2015.10 - 2016.3   Second semester

  • 創薬科学総論II

    2015.10 - 2016.3   Second semester

  • 薬理学I

    2015.10 - 2016.3   Second semester

  • 科学論文発表

    2015.4 - 2016.3   Full year

  • 先端研究実験II

    2015.4 - 2016.3   Full year

  • 先端研究実験I

    2015.4 - 2016.3   Full year

  • 薬学特別実習

    2015.4 - 2016.3   Full year

  • 卒業研究

    2015.4 - 2016.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2015.4 - 2016.3   Full year

  • 医療薬学演習I

    2015.4 - 2015.9   First semester

  • 医療薬学演習II

    2015.4 - 2015.9   First semester

  • 薬理学I

    2014.10 - 2015.3   Second semester

  • 総合医学III

    2014.10 - 2015.3   Second semester

  • 医療薬学系教育指導実習

    2014.10 - 2015.3   Second semester

  • 医療薬学研究

    2014.10 - 2015.3   Second semester

  • 薬学基礎実習IV

    2014.10 - 2015.3   Second semester

  • 薬学少人数ゼミナール

    2014.10 - 2015.3   Second semester

  • 創薬科学総論II

    2014.10 - 2015.3   Second semester

  • 卒業実習(アドバンスト実務実習)

    2014.4 - 2015.3   Full year

  • 英語科学討論

    2014.4 - 2015.3   Full year

  • 薬理・基礎理論

    2014.4 - 2015.3   Full year

  • 科学論文発表

    2014.4 - 2015.3   Full year

  • 先端研究実験II

    2014.4 - 2015.3   Full year

  • 先端研究実験I

    2014.4 - 2015.3   Full year

  • 薬学特別実習

    2014.4 - 2015.3   Full year

  • 卒業研究

    2014.4 - 2015.3   Full year

  • 薬理学III

    2014.4 - 2014.9   First semester

  • 医療薬学演習II

    2014.4 - 2014.9   First semester

  • 医療薬学演習I

    2014.4 - 2014.9   First semester

  • 薬理学I

    2013.10 - 2014.3   Second semester

  • 総合医学III

    2013.10 - 2014.3   Second semester

  • 薬理・薬理疾患治療

    2013.10 - 2014.3   Second semester

  • 薬学少人数ゼミナール

    2013.10 - 2014.3   Second semester

  • 医療薬学系教育指導実習

    2013.4 - 2014.3   Full year

  • 科学論文発表

    2013.4 - 2014.3   Full year

  • 先端研究実験II

    2013.4 - 2014.3   Full year

  • 先端研究実験I

    2013.4 - 2014.3   Full year

  • 卒業研究

    2013.4 - 2014.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2013.4 - 2014.3   Full year

  • 薬学特別実習

    2013.4 - 2014.3   Full year

  • 少人数セミナー

    2013.4 - 2013.9   First semester

  • 医療薬学演習II

    2013.4 - 2013.9   First semester

  • 医療薬学演習I

    2013.4 - 2013.9   First semester

  • コアセミナー

    2013.4 - 2013.9   First semester

  • 薬理学I

    2012.10 - 2013.3   Second semester

  • 総合医学III

    2012.10 - 2013.3   Second semester

  • 薬理・基礎理論

    2012.10 - 2013.3   Second semester

  • 薬学少人数ゼミナール

    2012.10 - 2013.3   Second semester

  • 医療薬学系教育指導実習

    2012.4 - 2013.3   Full year

  • 科学論文発表

    2012.4 - 2013.3   Full year

  • 先端研究実験II

    2012.4 - 2013.3   Full year

  • 先端研究実験I

    2012.4 - 2013.3   Full year

  • 卒業研究

    2012.4 - 2013.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2012.4 - 2013.3   Full year

  • 薬学特別実習

    2012.4 - 2013.3   Full year

  • 薬理学III

    2012.4 - 2012.9   First semester

  • 医療薬学演習II

    2012.4 - 2012.9   First semester

  • 医療薬学演習I

    2012.4 - 2012.9   First semester

  • 医薬品開発論

    2012.4 - 2012.9   First semester

  • 薬理学I

    2011.10 - 2012.3   Second semester

  • 薬学少人数ゼミナール

    2011.10 - 2012.3   Second semester

  • 総合医学III

    2011.10 - 2012.3   Second semester

  • 薬理・疾患治療

    2011.10 - 2012.3   Second semester

  • 薬学特別実習

    2011.4 - 2012.3   Full year

  • 医療薬学系教育指導実習

    2011.4 - 2012.3   Full year

  • 科学論文発表

    2011.4 - 2012.3   Full year

  • 先端研究実験II

    2011.4 - 2012.3   Full year

  • 先端研究実験I

    2011.4 - 2012.3   Full year

  • 卒業研究

    2011.4 - 2012.3   Full year

  • 卒業実習(アドバンスト実務実習)

    2011.4 - 2012.3   Full year

  • 薬理学III

    2011.4 - 2011.9   First semester

  • 医療薬学演習II

    2011.4 - 2011.9   First semester

  • 医療薬学演習I

    2011.4 - 2011.9   First semester

  • 医薬品開発論

    2011.4 - 2011.9   First semester

  • 英語科学討論

    2010.10 - 2011.3   Second semester

  • 総合医学III

    2010.10 - 2011.3   Second semester

  • 薬学少人数ゼミナール

    2010.10 - 2011.3   Second semester

  • 薬理学I

    2010.10 - 2011.3   Second semester

  • 薬理・基礎理論

    2010.10 - 2011.3   Second semester

  • 科学論文発表

    2010.4 - 2011.3   Full year

  • 先端研究実験I

    2010.4 - 2011.3   Full year

  • 医療薬学系教育指導実習

    2010.4 - 2010.9   First semester

  • 医療薬学演習I

    2010.4 - 2010.9   First semester

  • 薬理学I

    2009.10 - 2010.3   Second semester

  • 総合医学III(神経科学の最前線)

    2009.10 - 2010.3   Second semester

  • 薬理学ゼミ演習A又はB

    2009.4 - 2010.3   Full year

  • 薬理学III

    2009.4 - 2009.9   First semester

  • 高年次教養科目

    2009.4 - 2009.9   First semester

  • コアセミナー

    2009.4 - 2009.9   First semester

  • 薬理学I

    2008.10 - 2009.3   Second semester

  • 薬理学ゼミ演習A又はB

    2008.4 - 2009.3   Full year

  • 薬理学特論

    2008.4 - 2008.9   First semester

  • コアセミナー

    2008.4 - 2008.9   First semester

  • 薬品作用評価学I

    2007.10 - 2008.3   Second semester

  • 薬理学I

    2007.10 - 2008.3   Second semester

  • 薬理学ゼミ演習A又はB

    2007.4 - 2008.3   Full year

  • 薬理学II

    2007.4 - 2007.9   First semester

  • 薬品作用評価学I

    2006.10 - 2007.3   Second semester

  • 薬理学ゼミ演習A又はB

    2006.4 - 2007.3   Full year

  • 薬効解析学特論

    2006.4 - 2006.9   First semester

  • 医療薬学実習

    2006.4 - 2006.9   First semester

  • 薬理学II

    2006.4 - 2006.9   First semester

  • 薬理学ゼミ演習A又はB

    2005.4 - 2006.3   Full year

  • 医療薬学実習

    2005.4 - 2005.9   First semester

▼display all

FD Participation

  • 2025.1   Role:Participation   Title:第7回創薬産学官連携セミナー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2024.11   Role:Participation   Title:第6回創薬産学官連携セミナー(アカデミア創薬)

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2023.11   Role:Participation   Title:第2回薬学部局FD講演会「機関間連携」

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.11   Role:Participation   Title:アカデミア創薬

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.4   Role:Participation   Title:学生の多様性に対応した教育とは:障害学生への合理的配慮を中心に

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.4   Role:Participation   Title:学生の多様性に対応した教育とは:障害学生への合理的配慮を中心に

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.3   Role:Participation   Title:第3回創薬産学官連携(感染症研究拠点WG共催)セミナー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2021.9   Role:Participation   Title:JST 次世代研究者挑戦的研究プログラム説明会

    Organizer:University-wide

  • 2021.5   Role:Participation   Title:第2回創薬産学官連携セミナー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2021.2   Role:Participation   Title:先端医薬の品質・安全性確保と実用化のための科学―再生医療に用いる細胞加工製品を例に―,がんの個別化・精密医療の実現を目指した化学医学

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2020.9   Role:Participation   Title:M2B学習支援システム講習会

    Organizer:University-wide

  • 2019.8   Role:Participation   Title:外国人研究者・留学生受け入れ、貨物輸出と技術の提供に関して

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.11   Role:Participation   Title:Scopusの論文データを用いた薬学研究院の研究力分析

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.10   Role:Participation   Title:M2B/Moodleに関するFD

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2018.5   Role:Participation   Title:総合的創薬ソリューションプロバイダーによる創薬研究支援の新たな形 脂質改善薬の創製に向けた薬理学および分子生物学的研究

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2017.10   Role:Participation   Title:平成29年度馬出地区キャンパスFD「無意識のバイアスからの開放:ダイバーシティのススメ」

  • 2017.3   Role:Participation   Title:九州大学における情報セキュリティに関する取組

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2016.4   Role:Participation   Title:Webを用いた電子ポートフォリオの使用方法の概要について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.6   Role:Participation   Title:製薬業界の環境変化を受けた今後のMR活動とメディカルアフェアーズの確立について

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2009.10   Role:Participation   Title:OSCE評価者講習会

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2008.12   Role:Participation   Title:OSCEトライアル練習会

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2006.9   Role:Participation   Title:平成18年度FD薬学部企画

    Organizer:[Undergraduate school/graduate school/graduate faculty]

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Visiting, concurrent, or part-time lecturers at other universities, institutions, etc.

  • 2025  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2024  順天堂大学大学院環境医学研究所  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2023  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2022  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2021  京都大学  Classification:Part-time lecturer  Domestic/International Classification:Overseas 

  • 2020  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2019  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2018  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2017  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2016  順天堂大学大学院環境医学研究所  Classification:Affiliate faculty  Domestic/International Classification:Japan 

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Teaching Student Awards

  • 九州大学学生表彰

    Year and month of award:2025.3

    Classification of award-winning students:Undergraduate student   Name of award-winning student:栗野陽平

  • 九州大学学生表彰

    Year and month of award:2025.3

    Classification of award-winning students:Postgraduate student   Name of award-winning student:野巻昂平

  • 九州大学学生表彰

    Year and month of award:2025.3

    Classification of award-winning students:Doctoral student   Name of award-winning student:川邉陸

  • 学生優秀発表賞

    Year and month of award:2025.3

    Classification of award-winning students:Postgraduate student   Name of award-winning student:井絵理子

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  • 学生優秀発表賞

    Year and month of award:2025.3

    Classification of award-winning students:Postgraduate student   Name of award-winning student:角田昂大

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  • 学生優秀発表賞

    Year and month of award:2025.3

    Classification of award-winning students:Doctoral student   Name of award-winning student:藤森一樹

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  • 学生優秀発表賞

    Year and month of award:2025.3

    Classification of award-winning students:Postgraduate student   Name of award-winning student:野巻昂平

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  • Graduate Student Presentation Excellence Award

    Year and month of award:2025.3

    Classification of award-winning students:Doctoral student   Name of award-winning student:末藤大智

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  • Graduate Student Presentation Award

    Year and month of award:2025.3

    Classification of award-winning students:Postgraduate student   Name of award-winning student:野巻昂平

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  • 第46回日本疼痛学会 優秀演題賞

    Year and month of award:2024.11

    Classification of award-winning students:Doctoral student   Name of award-winning student:末藤大智

  • 第41回日本薬学会九州山口支部大会 優秀発表賞

    Year and month of award:2024.11

    Classification of award-winning students:Postgraduate student   Name of award-winning student:芝田悠人

  • 第77回日本薬理学会西南部会 若手優秀発表賞

    Year and month of award:2024.11

    Classification of award-winning students:Postgraduate student   Name of award-winning student:鍵山 一輝

  • 第77回日本薬理学会西南部会 若手優秀発表賞

    Year and month of award:2024.11

    Classification of award-winning students:Postgraduate student   Name of award-winning student:芝田悠人

  • 第23回次世代を担う若手のためのファーマ・バイオフォーラム2024 優秀発表賞

    Year and month of award:2024.9

    Classification of award-winning students:Postgraduate student   Name of award-winning student:鍵山一輝

  • 優秀賞

    Year and month of award:2024.7

    Classification of award-winning students:Postgraduate student   Name of award-winning student:野巻昂平

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  • 優秀賞

    Year and month of award:2024.7

    Classification of award-winning students:Doctoral student   Name of award-winning student:川邉陸

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  • 第97回日本薬理学会年会 優秀発表賞

    Year and month of award:2023.12

    Classification of award-winning students:Postgraduate student   Name of award-winning student:野巻昂平

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Other educational activity and Special note

  • 2021  Class Teacher  学部

  • 2015  Class Teacher  学部

  • 2013  Class Teacher  学部

Outline of Social Contribution and International Cooperation activities

  • Based on the results of basic research, we aim to contribute to society through pharmaceutical development, etc. We also conduct joint research with overseas research teams.

Social Activities

  • かゆみを感じる仕組み

    Role(s):Lecturer

    日本毒性学会  第21回市民公開セミナー  2024.7

  • Science Caféでの講演

    Science Japan  2022.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 明治学園高校での出前講義で高校生を対象に「薬理学~くすりはどのように効くの?~」というタイトルで薬学に関する模擬講義を行った。

    明治学園高校  北九州市  2022.4

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 市民公開講座「グリア細胞 脳を守る司令塔」

    日本学術振興会学術変革領域(A)グリアデコード,公益社団法人日本薬理学会,山梨GLIAセンター  福岡サンパレス  2022.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 模擬講義「薬理学 ~くすりはどのように効くの?~」

    明治学園高等学校  2021.7

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    Audience:Infants, Schoolchildren, Junior students, High school students

    Type:Seminar, workshop

  • 明治学園高校での出前講義で高校生を対象に「くすりの世界に入ってみませんか?」というタイトルで薬学に関する講義を行った。

    明治学園高校  明治学園高校  2019.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 広島大学薬学部が主催するヒロシマ薬剤師研修会にて「痛みを科学する~仕組みと治療~」に関する講演を行った。

    広島大学薬学部  広島  2019.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Seminar, workshop

  • 模擬講義「くすりの世界に入ってみませんか?」

    明治学園高等学校  2019.7

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    Audience:Infants, Schoolchildren, Junior students, High school students

    Type:Seminar, workshop

  • 「痛みとかゆみの慢性化メカニズムの解明に向けて」に関する講演

    九州大学日本橋サテライト開所記念式典  2018.2

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 「神経障害性疼痛メカニズムの基礎研究:グリア細胞からのアプローチ」に関する講演

    シオノギ製薬株式会社  2017.11

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 「痛みと痒み 最先端研究とアカデミア創薬 ~九大での取り組み~」に関する講演

    九州大学大学院薬学研究院 公開講座  2017.5

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 「痛みと痒みの慢性化メカニズムの研究」の講演

    日本ケミファ株式会社  2016.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 「痛みと痒みの慢性化メカニズムの研究」の講演

    東レ株式会社  2016.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 雑誌「あとぴナビ」へ掲載記事「アトピーの痒みは、なぜ慢性化するの?」に関する取材

    全国アトピー友の会  2015.9

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 日経バイオテク取材

    日経バイオテク  2015.5

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • ミクログリア転写因子IRF8を切り口にした慢性疼痛メカニズムの解明

    FIRST シンポジウム「科学技術が拓く2030 年  新宿  2014.2

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 平成25年度精神科薬物療法認定薬剤師講習会にて講演 「脳の神経伝達物質とその作用に関する基礎知識」

    日本病院薬剤師会  福岡  2014.2

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 読売新聞記事「神経の痛み 脊髄たんぱく質増加原因」にコメントを提供

    読売新聞  2013.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Newspaper, magazine

  • 慢性疼痛におけるミクログリア転写因子IRF8の役割

    「九州大学高等研究院若手研究者交流セミナー」  九州大学医学部百年講堂  2012.11

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Seminar, workshop

  • 第8回名古屋脊椎脊髄セミナー 「脊髄グリア細胞から神経障害性疼痛のメカニズムを探る」

    名古屋大学整形外科,日本ストライカー  名古屋  2011.7

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 第4回愛媛神経治療研究会 「グリア細胞から見えてきた神経障害性疼痛のメカニズム~グリア創薬を目指して~」

    愛媛大学,グラクソ・スミスクライン株式会社  愛媛  2011.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 高校生向け進学雑誌「薬系進学」にて「慢性痛など神経疾患メカニズムをグリア細胞から紐解く。新薬開発、そして既存薬から新しい作用を探索する「エコファーマ」を実践」というタイトルで研究室の紹介を行った。

    NEORICH  九州大学薬学部  2011.5

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 脊髄ミクログリアのATP受容体を介する疼痛制御

    ATPシグナリングとケミカルセンス  岡山  2011.1

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Seminar, workshop

  • グリア細胞から見えてきた難治性疼痛のメカニズム

    第11回群馬ペインクリニック懇話会  群馬  2010.11

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • ‘良い痛み’と‘悪い痛み’~その仕組みを考える~

    薬学部サマースクール  福岡  2010.8

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 福大付属大濠高等学校にて九大薬学部を説明

    九大薬学部  福岡  2010.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 慢性疼痛メカニズムの解明に向けて~グリア細胞からのアプローチ~

    平成22 年度福岡大学総合科学研究チームⅣ「細胞容積調節と心疾患治療薬」研究チーム主催研究会  福岡  2010.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • Role of Spinal Glial Cells in the Pathogenesis of Neuropathic Pain

    第14回脊椎と神経を語る会  東京  2010.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 脊髄グリア細胞:疼痛治療薬の新しい標的

    第12回北九州リハビリテーション医会  北九州  2009.11

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • ‘良い痛み’と‘悪い痛み’~その仕組みを考える~

    薬学部サマースクール  福岡  2009.8

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 我々の論文(PNAS 106: 8032-8037, 2009)に関する研究成果を日本神経科学学会の高校生・一般向けの項目(http://www.jnss.org/japanese/general/090612.html)で「モルヒネも効かない慢性疼痛「神経障害性疼痛」はどうして起こるのか?」というタイトルで紹介した。

    日本神経科学学会  2009.6

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

  • 「‘良い痛み’と‘悪い痛み’~その仕組みを考える~」というタイトルで講演した

    身の回りの毒に強くなる会  九州大学西新プラザ  2008.11

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Seminar, workshop

  • 脊髄グリア細胞と神経因性疼痛

    第10回Macnab Memorial Lecture  福島  2008.9

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 「痛みの克服に向けて」についての講演

    九州大学薬学研究院  九大コラボステーションI 視聴覚ホール  2008.5

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

  • 平成14年度創薬等ヒューマンサイエンス総合研究推進事業 研究成果等普及啓発事業 「痛みはどのようにして引き起こされるのか?-新しい鎮痛薬の可能性を求めて」

    主催:(財)ヒューマンサイエンス振興財団  東京慈恵会医科大学  2003.3

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Lecture

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Media Coverage

  • NHKニュース(全国:2022/5/12 14:00~14:05),ABEMA(テレビ朝日)ABEMAヒルズ(2022/5/20 12:00~13:10,かゆみには"タンパク質"が原因?),朝日新聞 2022.5.17夕刊(社会4面)かくと増すかゆみ 原因はたんぱく質 九大 メカニズム解明,科学新聞2022/5/20「慢性的なかゆみ」ひっかくとNPTX2タンパク質が増加 九大が悪循環の仕組み解明」,JIJI.COM,マイナビニュース,BIGLOBEニュース,exciteニュース,日経バイオテク,朝日新聞,日本経済新聞,QLifePro,日刊工業新聞,ニュースイッチ,時事メディカル,gooニュース,Medical Tribune,NHK NEWS WEB,日刊ゲンダイDIGITAL,Yahoo!ニュース,FNNプライムオンライン(フジテレビ),Yahoo!ニュース,科学新聞,Science Portal,Yahoo!ニュースなど TV or radio program

    NHK(全国),ABEMA(テレビ朝日),朝日新聞,科学新聞など  2023.5

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    NHKニュース(全国:2022/5/12 14:00~14:05),ABEMA(テレビ朝日)ABEMAヒルズ(2022/5/20 12:00~13:10,かゆみには"タンパク質"が原因?),朝日新聞 2022.5.17夕刊(社会4面)かくと増すかゆみ 原因はたんぱく質 九大 メカニズム解明,科学新聞2022/5/20「慢性的なかゆみ」ひっかくとNPTX2タンパク質が増加 九大が悪循環の仕組み解明」,JIJI.COM,マイナビニュース,BIGLOBEニュース,exciteニュース,日経バイオテク,朝日新聞,日本経済新聞,QLifePro,日刊工業新聞,ニュースイッチ,時事メディカル,gooニュース,Medical Tribune,NHK NEWS WEB,日刊ゲンダイDIGITAL,Yahoo!ニュース,FNNプライムオンライン(フジテレビ),Yahoo!ニュース,科学新聞,Science Portal,Yahoo!ニュースなど

  • ガリレオX(2023/3/12,19 11:30~12:00,11:30~12:00)「アレルギー研究最前線 抑え込み,治すことはできるのか?」に出演し,研究成果を紹介した。 TV or radio program

    BSフジ  2023.3

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    ガリレオX(2023/3/12,19 11:30~12:00,11:30~12:00)「アレルギー研究最前線 抑え込み,治すことはできるのか?」に出演し,研究成果を紹介した。

  • あしたが変わるトリセツショー(2023/1/19,26 19:57~20:42,15:10~15:55)「正しい保湿術!冬の乾燥に負けないかゆみ撃退法」で研究内容が紹介された。 TV or radio program

    NHK  2023.1

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    あしたが変わるトリセツショー(2023/1/19,26 19:57~20:42,15:10~15:55)「正しい保湿術!冬の乾燥に負けないかゆみ撃退法」で研究内容が紹介された。

  • 読売新聞(全国)「慢性の痛み 鎮める細胞 九大チーム マウスで発見」;西日本新聞「神経痛 緩和する細胞 世界初,九大研究チームが発見」;Yahoo!ニュース,読売新聞オンライン,dmenuニュース「けが治っても続く痛み「慢性疼痛」、軽減させる細胞発見…治療薬開発へ期待」;マイナビニュース他「慢性疼痛の痛みを自然に和らげていく細胞、九大などが発見」;西日本新聞me「神経性疼痛和らげる細胞、九大研究チームが発見 帯状疱疹や糖尿病患者の治療薬開発期待」;医療NEWS QlifePro「ミクログリア細胞が変化し、慢性疼痛を自然回復させることを発見-九大ほか」 Newspaper, magazine

    読売新聞(全国), 西日本新聞,Yahoo!ニュース,読売新聞オンライン,マイナビニュース,西日本新聞meなど  2022.4

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    読売新聞(全国)「慢性の痛み 鎮める細胞 九大チーム マウスで発見」;西日本新聞「神経痛 緩和する細胞 世界初,九大研究チームが発見」;Yahoo!ニュース,読売新聞オンライン,dmenuニュース「けが治っても続く痛み「慢性疼痛」、軽減させる細胞発見…治療薬開発へ期待」;マイナビニュース他「慢性疼痛の痛みを自然に和らげていく細胞、九大などが発見」;西日本新聞me「神経性疼痛和らげる細胞、九大研究チームが発見 帯状疱疹や糖尿病患者の治療薬開発期待」;医療NEWS QlifePro「ミクログリア細胞が変化し、慢性疼痛を自然回復させることを発見-九大ほか」

  • 科学新聞(紙面・オンライン)「触っただけで痛み」アロディニアはNPY神経細胞の活動低下が原因;Science Japan「Troublesome pain for which morphine is ineffective shown to be caused by decline in NPY nerve cell activity」 Newspaper, magazine

    科学新聞(紙面・オンライン),Science Japan  2021.1

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    科学新聞(紙面・オンライン)「触っただけで痛み」アロディニアはNPY神経細胞の活動低下が原因;Science Japan「Troublesome pain for which morphine is ineffective shown to be caused by decline in NPY nerve cell activity」

  • NHK福岡 NHKニュース おはよう日本(2020/10/6 6:00~7:00),NHK福岡 NHKニュース おはよう日本(2020/10/6 7:00~8:00),NHK福岡 ロクいち!福岡(2020/10/6 18:10~19:00),RKBラジオ櫻井浩二インサイト(2020/10/21 7:00~8:00 スペシャル・インサイト(7:40~7:50生放送)) 宮崎日日新聞(2020/10/6 朝刊総合2)「痛み強める細胞発見」,静岡新聞(020/10/6 朝刊23ページ)「痛み強める細胞発見」,日経産業新聞(2020/10/9)「九大,痛み強める神経細胞発見」,科学新聞(2020/10/16 4ページ)「脊髄内に新規アストロサイト発見 「定説と逆」痛み強める作用 九大 鎮痛薬開発に期待」,毎日新聞(2020/10/22 朝刊13ページ(全国版))「脊髄内細胞,痛みを強化 九大発見,痛覚の定説に一石」,オンライン:毎日新聞,Yahoo!JAPAN,msnニュース,共同通信,47 NEWS,Yahoo!JAPAN,東京新聞,西日本新聞,宮崎日日新聞,沖縄タイムス+プラス,アジア経済ニュース,中日新聞,So-net,秋田魁新報,徳島新聞,高知新聞,神戸新聞,静岡新聞,山梨日日新聞電子版,山形新聞,琉球新報,北日本新聞,Infoseekニュース,佐賀新聞LIVE,京都新聞,北海道新聞,福島民友新聞,山陰中央新報,山陽新聞,岐阜新聞Web,gooニュース TV or radio program

    NHK,RKBラジオ,毎日新聞,日経産業新聞  2021.1

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    NHK福岡 NHKニュース おはよう日本(2020/10/6 6:00~7:00),NHK福岡 NHKニュース おはよう日本(2020/10/6 7:00~8:00),NHK福岡 ロクいち!福岡(2020/10/6 18:10~19:00),RKBラジオ櫻井浩二インサイト(2020/10/21 7:00~8:00 スペシャル・インサイト(7:40~7:50生放送))
    宮崎日日新聞(2020/10/6 朝刊総合2)「痛み強める細胞発見」,静岡新聞(020/10/6 朝刊23ページ)「痛み強める細胞発見」,日経産業新聞(2020/10/9)「九大,痛み強める神経細胞発見」,科学新聞(2020/10/16 4ページ)「脊髄内に新規アストロサイト発見 「定説と逆」痛み強める作用 九大 鎮痛薬開発に期待」,毎日新聞(2020/10/22 朝刊13ページ(全国版))「脊髄内細胞,痛みを強化 九大発見,痛覚の定説に一石」,オンライン:毎日新聞,Yahoo!JAPAN,msnニュース,共同通信,47 NEWS,Yahoo!JAPAN,東京新聞,西日本新聞,宮崎日日新聞,沖縄タイムス+プラス,アジア経済ニュース,中日新聞,So-net,秋田魁新報,徳島新聞,高知新聞,神戸新聞,静岡新聞,山梨日日新聞電子版,山形新聞,琉球新報,北日本新聞,Infoseekニュース,佐賀新聞LIVE,京都新聞,北海道新聞,福島民友新聞,山陰中央新報,山陽新聞,岐阜新聞Web,gooニュース

  • RKB毎日放送「今日感テレビ」(2019/11/28 18:15~19:00)「かゆみ強まる仕組み 九大など発見」 TNCテレビ西日本「ももち浜S特報ライブ」(2019/11/28 16:50~19:00)「かゆみ強まるメカニズム 九大などが発見 教授「新薬開発につなげたい」福岡県」 Yahoo! Japan,Gooニュース (2019/11/28)「かゆみ強まるメカニズム 九大などが発見 教授「新薬開発につなげたい」福岡県 TV or radio program

    RKB毎日放送,TNCテレビ西日本,Yahoo! Japan,Gooニュース  2019.11

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    RKB毎日放送「今日感テレビ」(2019/11/28 18:15~19:00)「かゆみ強まる仕組み 九大など発見」
    TNCテレビ西日本「ももち浜S特報ライブ」(2019/11/28 16:50~19:00)「かゆみ強まるメカニズム 九大などが発見 教授「新薬開発につなげたい」福岡県」
    Yahoo! Japan,Gooニュース (2019/11/28)「かゆみ強まるメカニズム 九大などが発見 教授「新薬開発につなげたい」福岡県

  • アトピーのかゆみ:脊椎細胞活性化が原因 九大が解明 など

    毎日新聞 日本経済新聞 共同通信 朝日新聞デジタル 産経ニュース Yahoo!ニュース YOMIURI ONLINE 佐賀新聞LIVE 47 NEWS 西日本新聞 マイナビニュース exciteニュース 静岡新聞NEWS どうしんウェブ 京都新聞  2015.7

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    アトピーのかゆみ:脊椎細胞活性化が原因 九大が解明
    など

  • かゆみ増幅 細胞特定 九大,アトピー治療に期待 Newspaper, magazine

    日本経済新聞  2015.7

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    かゆみ増幅 細胞特定 九大,アトピー治療に期待

  • かゆみ増幅の細胞特定 九⼤院,アトピー治療に期待 Newspaper, magazine

    産経新聞  2015.7

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    かゆみ増幅の細胞特定 九⼤院,アトピー治療に期待

  • アトピーのかゆみ解明 九大,脳内細胞が作用 Newspaper, magazine

    日本経済産業新聞  2015.7

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    アトピーのかゆみ解明 九大,脳内細胞が作用

  • ロクいち福岡 「アトピー性皮膚炎でかゆみの仕組み新発見」 TV or radio program

    NHK福岡  2015.7

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    ロクいち福岡 「アトピー性皮膚炎でかゆみの仕組み新発見」

  • 今日感テレビ 「かゆみの原因を特定 “アトピー”治療で新発見」 TV or radio program

    RKB毎日放送  2015.7

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    今日感テレビ 「かゆみの原因を特定 “アトピー”治療で新発見」

  • めんたいPlus 「九大の研究グループ アトピーの「かゆみ」原因細胞を特定」 TV or radio program

    FBS福岡放送  2015.7

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    めんたいPlus 「九大の研究グループ アトピーの「かゆみ」原因細胞を特定」

  • あさチャン! 「アトピー“かゆみの原因”特定」 TV or radio program

    TBSテレビ  2015.7

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    あさチャン! 「アトピー“かゆみの原因”特定」

  • 慢性的かゆみ 仕組みを発見 九大教授ら 神経系細胞が関係 Newspaper, magazine

    読売新聞  2015.7

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    慢性的かゆみ 仕組みを発見 九大教授ら 神経系細胞が関係

  • アトピー かゆみ原因特定 九大グループ Newspaper, magazine

    毎日新聞  2015.7

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    アトピー かゆみ原因特定 九大グループ

  • アトピーのかゆみ 原因は神経系細胞 九大など,マウス実験で解明 Newspaper, magazine

    朝日新聞  2015.7

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    アトピーのかゆみ 原因は神経系細胞 九大など,マウス実験で解明

  • グリーンファルマ研究所について TV or radio program

    NHK,TNC,KBC,FBS  2015.5

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    グリーンファルマ研究所について

  • 既存薬から新薬 Newspaper, magazine

    西日本新聞  2015.5

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    既存薬から新薬

  • 九大に創薬拠点 既存薬の新たな効果も探る Newspaper, magazine

    朝日新聞WEB  2015.5

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    九大に創薬拠点 既存薬の新たな効果も探る

  • 創薬 九大が新戦略 Newspaper, magazine

    朝日新聞  2015.5

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    創薬 九大が新戦略

  • 新たな創薬拠点 九大病院に開設 Newspaper, magazine

    読売新聞  2015.5

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    新たな創薬拠点 九大病院に開設

  • 既存薬から新薬 九大拠点に研究所開設,全国初

    西日本新聞経済電子版  2015.5

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    既存薬から新薬 九大拠点に研究所開設,全国初

  • 「既存薬から新薬 九大拠点」 Newspaper, magazine

    西日本新聞  2015.5

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    「既存薬から新薬 九大拠点」

  • 転写因子IRF5は神経性障害性疼痛を引き起こすP2X4R+反応性ミクログリアを駆動する

    Nature Japan  2014.6

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    転写因子IRF5は神経性障害性疼痛を引き起こすP2X4R+反応性ミクログリアを駆動する

  • 難治性疼痛 原因物質特定 九大薬学部グループ 痛み緩和の可能性も Newspaper, magazine

    読売新聞  2014.5

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    難治性疼痛 原因物質特定 九大薬学部グループ 痛み緩和の可能性も

  • 熱烈発信!福岡NOW (18:20~19:00)および首都圏ニュース845(20:45~21:00)) 「神経ダメージで発症 “痛みの原因タンパク質突き止めた”」 TV or radio program

    NHK福岡  2014.5

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    熱烈発信!福岡NOW (18:20~19:00)および首都圏ニュース845(20:45~21:00))
    「神経ダメージで発症 “痛みの原因タンパク質突き止めた”」

  • 九大など、慢性疼痛の原因タンパク質が「IRF5」であることを究明

    マイナビニュース,Yahooニュース,Gooニュース,Livedoorニュース  2014.5

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    九大など、慢性疼痛の原因タンパク質が「IRF5」であることを究明

  • 神経障害性疼痛を解明、新薬に道開く

    SciencePortal  2014.5

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    神経障害性疼痛を解明、新薬に道開く

  • 九大,神経障害性疼痛の原因たんぱく質を新たに特定

    日刊工業新聞  2014.5

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    九大,神経障害性疼痛の原因たんぱく質を新たに特定

  • 難治性疼痛の原因物質発見,九大薬学部グループ

    YOMIURI ONLINE  2014.5

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    難治性疼痛の原因物質発見,九大薬学部グループ

  • 九大,神経障害性疼痛の仕組みを解明

    日本経済新聞  2014.5

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    九大,神経障害性疼痛の仕組みを解明

  • 神経障害性疼痛の原因タンパク質の特定 Newspaper, magazine

    西日本新聞  2014.5

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    神経障害性疼痛の原因タンパク質の特定

  • 鎮痛剤効きにくい神経性疼痛痛 九大,たんぱく質特定 新薬に道 Newspaper, magazine

    日本経済新聞  2014.5

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    鎮痛剤効きにくい神経性疼痛痛 九大,たんぱく質特定 新薬に道

  • がん・糖尿病で神経障害 激痛の原因物質特定 九大 Newspaper, magazine

    日本経済新聞  2012.4

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    がん・糖尿病で神経障害 激痛の原因物質特定 九大

  • 原因物質解明、九大チーム 「神経障害性疼痛」

    福島民報  2012.4

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    原因物質解明、九大チーム 「神経障害性疼痛」

  • 痛みの原因物質を特定

    SciencePortal  2012.4

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    痛みの原因物質を特定

  • 神経障害性疼痛」の原因物質を解明、九大チーム

    msn 産経ニュース  2012.4

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    神経障害性疼痛」の原因物質を解明、九大チーム

  • 九大など,神経障害性疼痛が引き起こされる仕組みを解明

    マイナビニュース,Yahoo! JAPANニュース,Infoseek楽天ニュース,Gooニュース  2012.4

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    九大など,神経障害性疼痛が引き起こされる仕組みを解明

  • 難治性疼痛新薬へ一歩、たんぱく質の関与特定

    YOMIURI ONLINE  2012.4

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    難治性疼痛新薬へ一歩、たんぱく質の関与特定

  • がん・糖尿病で神経損傷、激痛の原因物質特定 九大など Newspaper, magazine

    日本経済新聞  2012.4

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    がん・糖尿病で神経損傷、激痛の原因物質特定 九大など

  • 神経障害性疼痛:原因たんぱく質を特定、治療に光 九州大

    毎日jp,Yahoo! JAPANニュース,Exciteニュース  2012.4

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    神経障害性疼痛:原因たんぱく質を特定、治療に光 九州大

  • 慢性の激痛 「鍵」発見 脳・脊髄の細胞内で生成 九大など Newspaper, magazine

    日経産業新聞  2012.4

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    慢性の激痛 「鍵」発見 脳・脊髄の細胞内で生成 九大など

  • 神経障害性疼痛 仕組みを解明 九大グループ 治療薬開発へ期待 Newspaper, magazine

    西日本新聞  2012.4

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    神経障害性疼痛 仕組みを解明 九大グループ 治療薬開発へ期待

  • 神経性激痛 主犯格みつけた  九大が特定 既存薬で抑制へ前進 Newspaper, magazine

    朝日新聞  2012.4

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    神経性激痛 主犯格みつけた  九大が特定 既存薬で抑制へ前進

  • 神経障害性疼痛の原因特定 脊髄内たんぱく質が誘導 九大グループ Newspaper, magazine

    読売新聞  2012.4

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    神経障害性疼痛の原因特定 脊髄内たんぱく質が誘導 九大グループ

  • 神経障害性疼痛 治療に光 九大薬学研究院 原因たんぱく質特定 Newspaper, magazine

    毎日新聞  2012.4

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    神経障害性疼痛 治療に光 九大薬学研究院 原因たんぱく質特定

  • 日本経済新聞「ナゾ謎 かがく」欄で,「激しい痛みはなぜ起きる?」というタイトルで,薬理学分野での神経障害性疼痛に関する研究内容が掲載された Newspaper, magazine

    日本経済新聞  2012.2

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    日本経済新聞「ナゾ謎 かがく」欄で,「激しい痛みはなぜ起きる?」というタイトルで,薬理学分野での神経障害性疼痛に関する研究内容が掲載された

  • PNAS誌に掲載された論文「IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain」に関する内容 Newspaper, magazine

    朝日新聞,毎日新聞,読売新聞,日本経済産業新聞,および共同通信社,西日本新聞,東京新聞など多くの地方新聞  2009.5

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    PNAS誌に掲載された論文「IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain」に関する内容

  • PNAS誌に掲載された論文「IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain」に関する内容 TV or radio program

    NHK  2009.4

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    PNAS誌に掲載された論文「IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain」に関する内容

  • テレビ番組「サイエンスZERO」第200回「脳の知られざる主役 グリア細胞」で研究内容を紹介した. TV or radio program

    NHK教育  2008.3

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    テレビ番組「サイエンスZERO」第200回「脳の知られざる主役 グリア細胞」で研究内容を紹介した.

  • 研究成果「抗うつ薬パロキセチンが動物でもヒトでも神経因性疼痛を抑制すること」に関する内容 Newspaper, magazine

    共同通信社,および地方新聞社47社  2008.2

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    研究成果「抗うつ薬パロキセチンが動物でもヒトでも神経因性疼痛を抑制すること」に関する内容

  • Nature誌に掲載された論文「UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis」に関する内容 TV or radio program

    NHK  2007.4

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    Nature誌に掲載された論文「UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis」に関する内容

  • Nature誌に掲載された論文「UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis」に関する内容 Newspaper, magazine

    毎日新聞,読売新聞,日本経済産業新聞,共同通信社,西日本新聞,東京新聞,京都新聞,神戸新聞,茨城新聞,北海道新聞  2007.4

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    Nature誌に掲載された論文「UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis」に関する内容

  • ATP刺激により放出されるミクログリア由来疼痛関連因子として脳由来神経栄養因子を同定した. Newspaper, magazine

    読売新聞  2005.12

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    ATP刺激により放出されるミクログリア由来疼痛関連因子として脳由来神経栄養因子を同定した.

  • 難治性疼痛の発症および維持にATP受容体P2X4タンパクが関与している.新しい鎮痛薬の標的として注目される. Newspaper, magazine

    朝日,毎日,読売,BBC英国放送  2003.8

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    難治性疼痛の発症および維持にATP受容体P2X4タンパクが関与している.新しい鎮痛薬の標的として注目される.

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Activities contributing to policy formation, academic promotion, etc.

  • 2021.3   JST研究開発戦略センター(CRDS)

    JSTの研究開発戦略センター(CRDS)が発行している研究開発の俯瞰報告書の「ライフサイエンス・臨床医学分野(2021年)」で「感覚器科学」の分担作成をした。

  • 2018.8 - 2018.10   JSTの研究開発戦略センター(CRDS)

    JSTの研究開発戦略センター(CRDS)が発行している研究開発の俯瞰報告書の「ライフサイエンス・臨床医学分野(2019年)」で「感覚器科学」の分担作成をした。

Acceptance of Foreign Researchers, etc.

  • The Hebrew University of Jerusalem

    Acceptance period: 2023.4   (Period):2weeks to less than 1 month

    Nationality:Israel

  • Acceptance period: 2017.12   (Period):Less than 2 weeks

    Nationality:United Kingdom

  • トロント大学

    Acceptance period: 2017.3   (Period):2weeks to less than 1 month

    Nationality:Canada

  • トロント大学・トロント小児病院

    Acceptance period: 2016.3   (Period):Less than 2 weeks

    Nationality:Canada

  • トロント大学

    Acceptance period: 2015.3   (Period):2weeks to less than 1 month

    Nationality:Canada

    Business entity:On-campus funds

  • トロント大学,トロント小児病院

    Acceptance period: 2014.1 - 2015.1   (Period):Less than 2 weeks

    Nationality:Canada

    Business entity:On-campus funds

  • Acceptance period: 2007.3 - 2007.5   (Period):1 month or more

    Nationality:Germany

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Travel Abroad

  • 2018.8

    Staying countory name 1:Canada   Staying institution name 1:Hospital for Sick Children

  • 2016.11

    Staying countory name 1:United States   Staying institution name 1:ジョンズホプキンス大学

  • 2016.6

    Staying countory name 1:United States   Staying institution name 1:Keystone

  • 2016.3

    Staying countory name 1:Canada   Staying institution name 1:University of Toronto / Hospital for Sick Children

  • 2015.11

    Staying countory name 1:Taiwan, Province of China   Staying institution name 1:台北医科大学

  • 2013.5

    Staying countory name 1:Canada   Staying institution name 1:University of Calgary

  • 2012.3

    Staying countory name 1:Singapore   Staying institution name 1:National University of Singapore

  • 2011.3

    Staying countory name 1:United States   Staying institution name 1:Brigham & Women's Hospital Harvard Medical School

    Staying countory name 2:Canada   Staying institution name 2:Hospital for Sick Children

  • 2011.2

    Staying countory name 1:Australia   Staying institution name 1:Sydney University

  • 2010.3

    Staying countory name 1:Australia   Staying institution name 1:Sydney University

  • 2002.4 - 2004.3

    Staying countory name 1:Canada   Staying institution name 1:Programme in Brain and Behaviour, Hospital for Sick Children

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Notable Clinical Activities

  • がん性疼痛などの慢性疼痛,緩和医療領域において,医師あるいは薬剤師を対象に,その育成に貢献している。