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MAMI NODA Last modified date:2018.07.04



Undergraduate School


E-Mail
Homepage
http://seiri.phar.kyushu-u.ac.jp/English_index.html
Laboratory of Pathophysiology .
Phone
092-642-6554
Fax
092-642-6554
Academic Degree
Ph.D.
Field of Specialization
electrophysiology, cell biology, receptor, ion channel
Outline Activities
In the Laboratory of Pathophysiology, we are investigating the cellular mechanism of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. The main theme of our research are as follows;
1) Neuron-glial interaction and the role of glial cells in neurodegeneration. Glial cells, especially microglia, are rapidly activated even in minor pathological changes and play an important role in brain pathology. They express various neurotransmitter receptors, transporters and ion channels, though many of them are not known yet. We have identified AMPA/KA type of glutamate receptors, glutamate transporters and bradykinin receptors in rat microglia. Analyzing the role of these microglial membrane proteins will contribute to the better understanding of the neurodegenerative diseases and developing a new therapeutic strategy.
2) Regulation of neurotransmission by ubiquitin-proteasome system. Ubiquitin-proteasome system plays an important role in critical pathways including the cell cycle, morphogenesis of neural networks, down-regulation of cell surface receptors and ion channels. We are investigating the role of parkin and ubiquitin C terminal hydrolase, whose mutations are reported in familial Parkinson遮a disease, by transfecting their wild and mutant cDNAs into neuronal cell lines. These analyses will help understand the cellular mechanisms how neurodegenerations in Parkinson遮 disease occur and how to prevent them.
3) Anti-oxidative stress in model animals of neurodegeneration.
We are trying to find evidences for the benefits of taking anti-oxidative liquid using Parkinson’s disease model mice.
4) Social behavior-related hormones and brain function
We are trying to investigate expression and function of some hormones related to social behavior in the brain. Dysfunction of these hormones may explain some psychological disorders including autism.

Research
Research Interests
  • Protective effects of plasmalogen on damaged skin
    keyword : plasmalogen, skin, pressure ulcer, atopic dermatisis
    2018.04~2020.03.
  • Interaction between endocrine system and brain function via thyroid hormone
    keyword : thyroid hormone, microglia, astrocytes, neuronal dendritic spine, hyperthyroidsim, hypothyroidism, dementia, depression
    2013.04~2019.03.
  • Mechanisms of neuroprotective role of molecular hydrogen
    keyword : molecular hydrogen, Parkinson's disease, Ischemia
    2006.04~2018.03.
  • Effects of polyphenols on brain cells.
    keyword : polyphnol, microglia, astrocytes, neurons
    2015.10~2018.09.
  • Mechanism of protective effect of deoxynucleic acid sodium salt on ischemia-reperfusion injury
    keyword : Derinat, ischemia-reperfusion, ROS, antioxidant
    2015.10~2017.03.
  • Effects of neuropeptides via microglia in the central nervous system
    keyword : microglia, neuropeptide, galanin, orexin
    2008.04~2016.03.
  • Role of AMPA-type of glutamate receptors in microglia
    keyword : microglia, AMPA receptor, GluR2, Alzheimer's disease
    2009.04~2015.03.
  • Mictroenvironment of brain metastasis of lung cancer
    keyword : lung caner, brain metastasis, astrocyte, cytokine, microglia
    2006.05~2018.03.
  • Molecular mechanismNeuron-glia-blood vessel interaction and new therapeutic targets
    keyword : microglia, astrocyte, patch-clamp method, central nervous system, ion channel, receptor, neuropeptide
    1999.04~2009.03Molecular and cellular analyses on the interaction of glia-neuron-blood vessels and new drug discovery: 1) The expession and function of neuropeptide receptors in microglia. 2) Cell biology of microglia; anayses of the ion channels, receptors, and the release of cytokine release. 3) Inflammation followed by trauma, ischemia and neurodegeneration. 4) Neuroprotective drugs targeting microglial receptor or ion channels. 5) The role of glial cells in brain metasiases of lunc cancer cells..
  • Effectis of anti-oxidants on neurodegenrative disorders
    keyword : MPTP model mice, Parkinson's disease, anti-oxidants, dopaminergic neurons, hydrogen
    2005.07~2009.03Anti-oxidative stress in model animals of neurodegeneration: We are trying to find evidences for the benefits of drinking hydrogen-containing water using MPTP Parkinson’s disease model mice. .
  • Brain function in the social behavior
    keyword : pituitary hormon, social behavior, autism, pcychological disorder, CD38
    2006.04~2009.03Social behavior-related hormones and brain function: We are trying to investigate expression and function of posterior pituitary hormones which are related to social behavior in the brain. Dysfunction of these hormones may explain some psychological disorders and pervasive developmental disorders including autism. .
  • The role of familial Parkinson's disease-related genes in physiological and pathophysiological functions
    keyword : Ubiquitin carboxy-terminal hydrolase L, parkin, patch-clamp method, neurotransmission, receptor
    2000.09~2009.03Physiological and pathophysiological analyses of the genes related to Parkinson's Disease. Electrophysiological analyses on the function of ubiquitin C-terminal hydrolase (UCH L1) and parkin in the neurotransmission. Pathophysiological effects of mutant form of UCH L1 and parkin..
Current and Past Project
  • Protective effects of plasmalogen agains skin damage in poressure ulcer and atopic dermatisis
  • Interaction between endocrina system, especially thyroid hormone, and brain's immune cells, microglia (Started as a collaboarion with State University of St. Petersburd, Russia).
    Animal model of hypothyroidism and mechanism of neuropsychiatric pathology (2018-2020, KAKEN-C, totally 4,980,000 JY)
    Molecular mechanism of dementia/psychiatric symptoms due to abnormal thyroid hormone (With University of Ljubljana (2018-2020.03; total 4,000,000 JY)
  • Mechanism of oxidative-stress-resistance against ischemic injury of optic nerve
  • The analyses of interaction between neuron, glia, and blood vessles via neuropeptides and neurotransmitters. Mutual communications between Max-Delbruck Center for Molecular Medicine (MDC) in Germany, University of Manchester (UK), University of the Basque Country(Spain), Krasnoyarsk State Medical University (Russia)and Federal University of Rio Grande do Sul (Brazil)are going on.
  • Effects of Derinat on ischemia-reperfusion (IR)-induced pressure ulcer mouse models are analysed and elucidate the mechanism of anti-inflammatory and anti-oxidative effects. (Started as a collaboration with Russian Academy for Experimental Medicine, St. Petersburg, Russsia, then Kaohsiung Medical University, Taiwan, joined. )
  • The incidence of brain metastasis is increasing, however, little is known about molecular mechanism responsible for lung cancer-derived brain metastasis and their development in the brain. Therefore, brain pathology is examined in an experimental model system of brain metastasis. In addition, the mechanism of immune evasion of lung cacer cells in the brain is also anayled at cellular level.
  • The mechanism how CD38-deficiency in microglia may also cause microglial dysfunction and contribute to behavioral deficits is investigated.
  • The role of glial cells in chronic fatigue is important. Therefore, the purpose of this project is to elucidate the interplay between astrocytes and microglia and how it affects neuronal functions.
  • Research on dysfunction in the maintainance of nucliotide pool in disease models
  • Functional Analyses of CD38 and cyclic ADP riblse at cellular level, especially in brain's immune cells.
  • 1) Ion channels and receptors in microglia
    2) Ion channels and receptors in astrocyte
    3) Interaction between microglia-astrocyte and neuron
    4) Interaction between microglia-astrocyte and blood vessels
  • Bradykinin is a potent mediator of inflammation and pain not only periphery but also in the central nervous system. We found that microglial cells express bradykinin receptors, though their functions are still elusive. To investigate the functional role of kinins in microglia is important to understand the inflammaroty diseases in the brain and could be a therapeutic targets.
  • KCNQ channels which are known to control the neuronal excitability have several subtypes, some of them are expressed also in heart and endothelial cells. We found that KCNQ3/5 are specifically expressed in astrocyte, micrglia, and C6 glioma cells. The KCNQ3/5 channel opener is reported to have neuroprotective effect in hypoxia. The investigation of the function of KCNQ channels in glial cells may help understand the mechanism of neuroprotection and contribute to make a new neuroprotective drug.
Academic Activities
Books
1. Mami Noda, Thyroid Hormone in the CNS: Contribution of Neuron-Glia Interaction. VH 106 Thyroid Hormone, ELSEVIER (2017), ELSEVIER, 2018.01.
2. Alexej Verkhratsky, MAMI NODA, Vladimir Parpura, Microglia: Structure and Function. In: Brain Mapping: An Encyclopedic Reference,
Arthur W. Toga (ed)
, Academic Press: Elsevier , vol. 2, pp. 109-113, 2015.01.
3. Alexei Verkhratsky, MAMI NODA, General Physiology and Pathophysiology of Microglia, in “Neuroinflammation and Neurodegeneration”, P.K. Peterson and M. Toborek (eds.), Springer Science+Business Media New York , p47-60 , 2014.08.
4. MAMI NODA, Chapter 13. Possible therapeutic targets in microglia, In: Pathological Potential of Neuroglia: Possible New Targets for Medical Intervention, p293-313, Vladimir Parpura and Alexei Verkhratsky (eds), MA: Springer , p293-313, 2014.07.
5. Alexei Verkhratsky, MAMI NODA, Vladimir Parpura, Sergei Kirischuk, Sodium fluxes and astroglial function, In: Advances in Experimental Medicine and Biology. Sodium Calcium Exchange: A Growing Spectrum of Pathophysiological Implications, L. Annunziato (ed.), Springer Science+Business Media New York , 961: 295-305., 2013.06.
6. MAMI NODA, Physiology of microglia, Neuroglia 3rd EditionPress, Oxford University Press, p223-237, 2012.10.
7. MAMI NODA, 3. The Brain Microenvironment. Brain and Central Nervous System Metasitasis, the Biological Basis and Clinical Considerations. , Springer, p43-54, 2012.09.
8. Mami Noda, Transporter Current Measurements. in "Modern Patch Clamp Techniques", Springer , p195-206, 2012.03.
9. Mami Noda, Glial Cells in Brain Defence Mechanisms. in "NeuroImmune Biology", Elsevier , Vol. 9, p161-167, 2011.06.
10. Noda M., Seike T., Fujita K., Kido M., Tanaka T., Iguchi H. , Adaptation Biology and Medicine, Narossa Publishing House. New Delhi, India. , The processes of adaptation of microglia in brain trauma and metastasis. Volume 5, p165-172., 2007.05.
Reports
1. Mami Noda, Microglia and its phagocytic abilities. 23(1): 11-18 (2017), Clinical Pathophysiology, 23(1): 11-18, 2017.06.
2. Mami Noda, Mechanisms of nicotine-induced neuroprotection: Inhibition of NADPH oxidase and subsequent proton channel activation by stimulating alpha 7 nicotinic acetylcholine receptor in activated microglia., Advances in Neuroimmune Biology, 10.3233/NIB-160119, 6 (2015/2016) 107–115, 2016.06.
3. MAMI NODA, Dysfunction of glutamate receptors in microglia may cause neurodegeneration. , Curr Alzheimer Res. , 2015.10.
4. MAMI NODA, Possible role of glial cells in the relationship between thyroid dysfunction and mental disorders. , Front. Cell. Neurosci. 9:194, 2015.06.
5. MAMI NODA, Ikuroh Ohsawa, Masafumi Ito, Kinji Ohno, Beneficial effects of hydrogen in the CNS and a new brain-stomach interaction., European Journal of Neurodegenerative Diseases , 3(1): 25-34 , 2014.12.
6. MAMI NODA, Kyota Fujita, Ikuroh Ohsawa, Masafumi Ito, Kinji Ohno, Multiple Effects of Molecular Hydrogen and its Distinct Mechanism. , Journal of Neurolog Disorders , 2:6, 2014.12, [URL].
7. MAMI NODA, Beppu K, Possible Contribution of Microglial Glutamate Receptors to Inflammatory Response upon Neurodegenerative Diseases., J Neurol Disord 1: 131. doi:10.4172/2329-6895.1000131 , 2013.11.
8. MAMI NODA, 井福 正隆, Mori Y, Verkhratsky A, Calcium Influx Through Reversed NCX Controls Migration of Microglia., Adv Exp Med Biol. , Noda M, Ifuku M, Mori Y, Verkhratsky A. , 2013.03, Microglia, the immune cells of the central nervous system (CNS), are busy and vigilant guards of the adult brain, which scan brain parenchyma for damage and activate in response to lesions. Release of danger signals/chemoattractants at the site of damage initiates microglial activation and stimulates migration. The main candidate for a chemoattractant sensed by microglia is adenosine triphosphate (ATP); however, many other substances can have similar effects. Some neuropeptides such as angiotensin II, bradykinin, endothelin, galanin and neurotensin are also chemoattractants for microglia. Among them, bradykinin increases microglial migration using mechanism distinct from that of ATP. Bradykinin-induced migration is controlled by a G(i/o)-protein-independent pathway, while ATP-induced migration involves G(i/o) proteins as well as mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)-dependent pathway. Galanin was reported to share certain signalling cascades with bradykinin; however, this overlap is only partial. Bradykinin, for example, stimulates Ca(2+) influx through the reversed Na(+)/Ca(2+) exchange (NCX), whereas galanin induces intracellular Ca(2+) mobilization by inositol-3,4,5-trisphosphate (InsP(3))-dependent Ca(2+) release from the intracellular store. These differences in signal cascades indicate that different chemoattractants such as ATP, bradykinin and galanin control distinct microglial functions in pathological conditions such as lesion and inflammation and NCX contributes to a special case of microglial migration..
9. Therapeutic approach to neurodegenerative diseases by medical gases: focusing of redox signaling and related antioxidant enzymes. .
10. Noda M, Fujita K, Chih-Hung Lee CH, Yoshioka T., The principle and the potential approach to ROS-dependent cytotoxicity by non-pharmaceutical
therapies: Optimal use of medical gases with antioxidant properties.
, Curr Pharm Design, 2011.07.
11. Noda M, Ifuku M, Okuno Y, Beppu K, Mori Y, Naoe S., Neuropeptides as Attractants of Immune Cells in the Brain and their Distinct Signaling.
, Advances in Neuroimmune Biology, 2011.07.
12. Fujita K, Nakabeppu Y, Noda M., Therapeutic effects of hydrogen in animal models of Parkinson’s disease. , Animal Model of Parkinson’s Disease, 2011.05.
13. Kettenmann H, Hanisch UW, Noda M, Verkhratsky A., Physiology of microglia, Physiol Rev., 2011.04.
14. Noda M, Sasaki K, Ifuku M, Wada K, Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects. , Neurochem. Int. , doi:10.1016/j.neuint.2007.06017. , 2007.09.
15. Noda M., Kettenmann H., Wada K., Anti-inflammatory effects of kinins via microglia in the central nervous system., Biol. Chem., 387: 167-171, 2006.01.
Papers
1. Noda M, Tomonaga D, Kitazono K, Yoshioka Y, Liu J, Rouseau JP, Kinkead R, Ruff MR, Pert CB. , Neuropathic pain inhibitor, RAP-103, is a potent inhibitor of microglial CCL1/CCR8. Neurochem Int. 2017 Dec 14. pii: S0197-0186(17)30474-6. doi: 10.1016/j.neuint.2017.12.005, Neurochem Int., 10.1016/j.neuint.2017.12.005, pii: S0197-0186(17)30474-6., 2017.12.
2. Yoshii Y, Inoue T, Sato T, Iwasaki Y, Kojima M, Yada T, Nakabeppu Y, Noda M. , Complexity of Stomach–Brain Interaction Induced by Molecular Hydrogen in Parkinson’s Disease Model Mice. , Neurochem Res, 10.1007/s11064-017-2281-1, 42, 9, 2658-2665, 2017.09.
3. Noda M. Kobayashi A., Nicotine inhibits activation of microglial proton currents via interactions with α7 acetylcholine receptors. J Physiol Sci. Jan;67(1):235-245 (2017), J Physiol Sci., 67, 1, 235-245, 2017.01, Alpha 7 subunits of nicotinic acetylcholine receptors (nAChRs) are expressed in microglia and are involved in the suppression of neuroinflammation. Over the past decade, many reports show beneficial effects of nicotine, though little is known about the mechanism. Here we show that nicotine inhibits lipopolysaccharide (LPS)induced proton (H?) currents and morphological change by using primary cultured microglia. The H? channel currents were measured by whole-cell patch clamp method under voltage-clamp condition. Increased H? current in activated microglia was attenuated by blocking NADPH oxidase. The inhibitory effect of nicotine was due to the activation of a7 nAChR, not a direct action on the H? channels, because the effects of nicotine was cancelled by a7 nAChR antagonists. Neurotoxic effect of LPS-activated microglia due to inflammatory cytokines was also attenuated by pretreatment of microglia with nicotine. These results suggest that a7 nAChRs in microglia may be a therapeutic target in neuroinflammatory diseases.
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4. Noda M, Mori Y, Yoshioka Y., Sex- and age-dependent effects of thyroid hormone on glial morphology and function. 2, 85-92 (2016), Opera Medica et Physiologica (OM&P), 2, 164-171, 2016.04, Thyroid hormones (THs) are essential for the development and function of the central nervous system (CNS), not only for neuronal cells but also for glial development and differentiation. In adult CNS, both hypo- and hyper-thyroidism may affect psychological condition and potentially increase the risk of cognitive impairment and neurodegeneration including Alzheimer’s disease (AD). We have reported non-genomic effects of tri-iodothyronine (T3) on microglial functions and its signaling in vitro (MORI et al., 2015). Here we report the effects of hyperthyroidism on glial cells in vivo using young and old male and female mice. Immunohistochemical analyses showed glial activation are sex- and age-dependent. We also injected fluorescent-labeled amyloid β peptide (Aβ1-42) intracranially to L-thyroxine (T4)–injected hyperthyroid model mice and observed sex-dependent microglial phagocytosis in vivo as well. These results may partly explain the gender- and age-dependent differences in neurological and psychological symptoms of thyroid dysfunction..
5. Yuki Mori, Daichi Tomonaga, Anastasia Kalashnikova, Fumihiko Furuya, Nozomi Akimoto, Masataka Ifuku, Yuki Okuno, Kaoru Beppu, Kyota Fujita, Toshihiko Katafuchi, Hiroki Shimura, Leonid P. Churilov, MAMI NODA, Effects of 3,3',5-triiodothyronine on microglial functions. , GLIA, DOI: 10.1002/glia.22792, 63, 906-920, 2015.01, L-tri-iodothyronine (3, 3’, 5–triiodothyronine; T3) is an active form of the thyroid hormone (TH) essential for the development
and function of the CNS. Though nongenomic effect of TH, its plasma membrane–bound receptor, and its signaling has
been identified, precise function in each cell type of the CNS remained to be investigated. Clearance of cell debris and apoptotic
cells by microglia phagocytosis is a critical step for the restoration of damaged neuron-glia networks. Here we report
nongenomic effects of T3 on microglial functions. Exposure to T3 increased migration, membrane ruffling and phagocytosis
of primary cultured mouse microglia. Injection of T3 together with stab wound attracted more microglia to the lesion site in
vivo. Blocking TH transporters and receptors (TRs) or TRa-knock-out (KO) suppressed T3-induced microglial migration and
morphological change. The T3-induced microglial migration or membrane ruffling was attenuated by inhibiting Gi/o-protein
as well as NO synthase, and subsequent signaling such as phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase
(MAPK)/extracellular signal-regulated kinase (ERK). Inhibitors for Na1/K1-ATPase, reverse mode of Na1/Ca21 exchanger
(NCX), and small-conductance Ca21-dependent K1 (SK) channel also attenuated microglial migration or phagocytosis. Interestingly,
T3-induced microglial migration, but not phagocytosis, was dependent on GABAA and GABAB receptors, though
GABA itself did not affect migratory aptitude. Our results demonstrate that T3 modulates multiple functional responses of
microglia via multiple complex mechanisms, which may contribute to physiological and/or pathophysiological functions of
the CNS..
6. MAMI NODA, Yuichiro Kojima, Fumiya Suematsu, Shirin Akther, Haruhiro Higashida, Expression of CD38 and Its Interaction with TRPM2 in Microglia, MESSENGER , doi:10.1166/msr.2014.1033, 3, 1-7, 2014.12, Using primary cultured mouse microglia, expression of CD38 was significantly up-regulated in lipopolysaccharide
(LPS, 100 ng/mL)-activated microglia, but not in adenosine triphosphate (ATP, 100 M)-treated microglia (24 h pretreatment).
Since TRPM2 (transient receptor potential cation channel, subfamily M, member 2) is highly expressed
in microglia and is activated by cADPR and ADPR, the effect of knock-down of TRPM2 using siRNA on the expression
of CD38 was examined in activated microglia. Unexpectedly, knock-down of TRPM2 significantly up-regulated
the expression of CD38. LPS-induced production of nitric oxide was not affected by TRPM2 siRNA, while release
of TNF- and IL-1 were attenuated by TRPM2 siRNA. These results suggest that CD38 may substitute for the
expression of TRPM2 when TRPM2 is absent or decreased and partially compensate the [Ca2+]i mobilization. Taking
account of the role of CD38, especially in activated microglia, dysfunction of CD38 could disturb Ca2+ signaling
in microglia as well and may lead to breakdown of the brain homeostasis..
7. Matsumoto A, Megumi Yamafuji, Tachibana T, Yusaku Nakabeppu, MAMI NODA, Nakaya H, Oral 'hydrogen water' induces neuroprotective ghrelin secretion in mice. , Sci Rep. , 10.1038/srep03273. , 3, 3273, 2013.11.
8. Nozomi Akimoto, Honda K, Uta D, Kaoru Beppu, Nakashima S, Matsuzaki Y, Ushijima Y, Mizuho A Kido, Imoto K, Takano Y, MAMI NODA, CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury., Cell Death Dis., 10.1038/cddis.2013.198. , 4, e679, 2013.06, Cytokines such as interleukins are known to be involved in the development of neuropathic pain through activation of neuroglia. However, the role of chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated T cells, in the nociceptive transmission remains unclear. We found that CCL-1 was upregulated in the spinal dorsal horn after partial sciatic nerve ligation. Therefore, we examined actions of recombinant CCL-1 on behavioural pain score, synaptic transmission, glial cell function and cytokine production in the spinal dorsal horn. Here we show that CCL-1 is one of the key mediators involved in the development of neuropathic pain. Expression of CCL-1 mRNA was mainly detected in the ipsilateral dorsal root ganglion, and the expression of specific CCL-1 receptor CCR-8 was upregulated in the superficial dorsal horn. Increased expression of CCR-8 was observed not only in neurons but also in microglia and astrocytes in the ipsilateral side. Recombinant CCL-1 injected intrathecally (i.t.) to naive mice induced allodynia, which was prevented by the supplemental addition of N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801. Patch-clamp recordings from spinal cord slices revealed that application of CCL-1 transiently enhanced excitatory synaptic transmission in the substantia gelatinosa (lamina II). In the long term, i.t. injection of CCL-1 induced phosphorylation of NMDA receptor subunit, NR1 and NR2B, in the spinal cord. Injection of CCL-1 also upregulated mRNA level of glial cell markers and proinflammatory cytokines (IL-1β, TNF-α and IL-6). The tactile allodynia induced by nerve ligation was attenuated by prophylactic and chronic administration of neutralizing antibody against CCL-1 and by knocking down of CCR-8. Our results indicate that CCL-1 is one of the key molecules in pathogenesis, and CCL-1/CCR-8 signaling system can be a potential target for drug development in the treatment for neuropathic pain..
9. MAMI NODA, Akimoto N, 井福 正隆, Mori Y, Effects of chemokine (C-C motif) ligand 1 on microglial function., Biochem Biophys Res Commun., 10.1016/j.bbrc.2013.05.126., 436, 3, 455-461, 2013.07, Microglia, which constitute the resident macrophages of the central nervous system (CNS), are generally considered as the primary immune cells in the brain and spinal cord. Microglial cells respond to various factors which are produced following nerve injury of multiple aetiologies and contribute to the development of neuronal disease. Chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated T cells, has been shown to play an important role in neuropathic pain induced by nerve injury and is also produced in various cell types in the CNS, especially in dorsal root ganglia (DRG). However, the role of CCL-1 in the CNS and the effects on microglia remains unclear. Here we showed the multiple effects of CCL-1 on microglia. We first showed that CCR-8, a specific receptor for CCL-1, was expressed on primary cultured microglia, as well as on astrocytes and neurons, and was upregulated in the presence of CCL-1. CCL-1 at concentration of 1 ng/ml induced chemotaxis, increased motility at a higher concentration (100 ng/ml), and increased proliferation and phagocytosis of cultured microglia. CCL-1 also activated microglia morphologically, promoted mRNA levels for brain-derived neurotrophic factor (BDNF) and IL-6, and increased the release of nitrite from microglia. These indicate that CCL-1 has a role as a mediator in neuron-glia interaction, which may contribute to the development of neurological diseases, especially in neuropathic pain..
10. Beppu K, Kosai Y, Mizuho A Kido, Akimoto N, Mori Y, Kojima Y, Fujita K, Okuno Y, Yamakawa Y, Ifuku M, Shinagawa R, Nabekura J, Sprengel R, MAMI NODA, Role of GluA2 (GluR-B) Subunit of AMPA-type of Glutamate Receptor in Microglia., GLIA, 10.1002/glia.22481., 61, 6, 881-891, 2013.06.
11. Akimoto N, Kamiyama Y, Yamafuji M, Fujita K, Seike T, Mizuho A Kido, Yokoyama S, Higashida H, MAMI NODA, Immunohistochemistry of CD38 in Different Cell Types in the Hypothalamus and Pituitary of Male Mice, Messenger, Volume 2, 2, 1-8, 2013.01, Oxytocin (OT) and arginine vasopressin (AVP) are neurohypophysial hormones. CD38 and cyclic ADP-ribose (cADPR) formation have been identified in the hypothalamus and are critical for OT, but not AVP, secretion, with profound consequential changes in social behaviors in mice. In the present study, we examined the immunolocalization of CD38, OT and AVP in different cell types in the hypothalamus and pituitary lobe of male mice. In the hypothalamus, CD38 immunoreactivity was found more commonly in OT neurons than AVP neurons. In the posterior pituitary lobe, the expression of CD38 was partly merged with OT and AVP, while pituicyte-like staining was also observed. In the CD38-deficient hypothalamus and posterior lobe, stronger staining of OT was observed, suggesting accumulation of OT due to lack of the releasing process, as reported previously. Co-expression of CD38 with glial cells showed that CD38 was rarely expressed in glial fibrillary acidic protein (GFAP)-positive astrocytes. However, expression of CD38 protein in microglia was detected and more expression of CD38 in microglia was observed in the lipopolysaccharide-injected mouse brain. The expression of CD38 in different cell types, especially in microglia, in the hypothalamus and pituitary may indicate functional roles of CD38 in brain's immune system as well as in neurohypophysial hormone release..
12. MAMI NODA, Yamakawa Y, matsunaga naoya, Naoe S, Jodoi T, Yamafuji M, Akimoto N, Teramoto N, Fujita K, shigehiro ohdo, Iguchi H, IL-6 Receptor Is a Possible Target against Growth of Metastasized Lung Tumor Cells in the Brain., Int J Mol Sci., 10.3390/ijms14010515 (2012), 14, 1, 515-526, 2012.12.
13. Ifuku M, Okuno Y, Yamakawa Y, Izum K, Seifert S, Kettenmann H, Noda M. , Functional importance of inositol-1,4,5-triphosphate-induced intracellular Ca2+ mobilization in galanin-induced microglial migration., J Neurochem., 117, 1, 61-70, 2011.04.
14. Noda M, Seike T, Fujita K, Yamakawa Y, Kido M, Iguchi H. , Role of Immune Cells in Brain Metastasis of Lung Cancer Cells and Neuron-Tumor Cell Interaction. , Neurosci Behav Physiol. , 41, 3, 243-51, 2011.03.
15. Seike T, Fujita K, Yamakawa Y, Kido MA, Takiguchi S, Teramoto N, Iguchi H, Noda M., Interaction between lung cancer cells and astrocytes via specific inflammatory cytokines in the microenvironment of brain metastasis., Clin Exp Metastasis. , 28(1):13-25 (2011, 1, 13-25, 2011.01.
16. Mami Noda, Effects of neuropeptides in microglia under pathophysiologic conditions. , Eighth Goettingen Meeting of German Neuroscience Society, 2009.03.
17. Yukiko Yamakawa, Kyota Fujita, Toshihiro Seike, Mizuho A. Kido, Haruo Iguchi and Mami Noda, Cytokine released from astrocytes promote proliferation of lung cancer cells in brain metastases, Berlin Brain Days; 5th International PhD Symposium, p90, 2008.12.
18. Yuko Okuno, Masataka Ifuku, Mami Noda, Effects of neuropeptide orexin on microglial migration., Berlin Brain Days; 5th International PhD Symposium, p87, 2008.12.
19. Kyota Fujita, Toshihiro Seike, Yukiko Yamakawa, Mizuki Ohno, Hiroo Yamaguchi, Hidetaka Yamada, Toshihiko Katafuchi, Atsushi Takaki, Mizuho Kido, Yusaku Nakabeppu and Mami Noda, Protective effects of hydrogen in drinking water in a mouse model of Parkinson’s disease., Berlin Brain Days; 5th International PhD Symposium, p80, 2008.12.
20. Masataka Ifuku, Yuko Okuno, Yukiko Yamakawa, Mami Noda, Galanin-induced migration and activation of microglia is mediated by galanin receptor 2 (GalR2) pathway. , Society for Neuroscience, 38th Annual Meeting, 637.29, 2008.11.
21. Mami Noda, Masataka Ifuku, Yuko Okuno, Yukiko Yamakawa, Brain’s immune cells and anti-inflammatory effects of neuropeptides, EHRLICH II 2nd World Conference on Magic Bullets, 1212, 2008.10.
22. Mami Noda, Masataka Ifuku, Yukiko Yamakawa, Yuko Okuno, Role of neuropeptide galanin in microglia, 6th FENS Forum , 148.9

, 2008.07.
23. Mami Noda, Toshihiro Seike, Kyouta Fujita, Mizuho A. Kido, and Haruo Iguchi, The role of glial cells in brain metastases of tumor cells, The 17th Interational Conference on Brain Tumor Research & Therapy, p32, 2008.06.
24. Amano T, Wada E, Yamada D, Zushida K, Maeno H, Noda M, Wada K, Sekiguchi M, Heightened Amygdala Long-Term Potentiation in Neurotensin Receptor Type-1 Knockout Mice. , Neuropsychopharmacology, 2008.03.
25. Ifuku M , Färber K, Okuno Y, Yamakawa Y, Miyamoto T, Nolte C, Merrino VF, Kita S, Iwamoto T, Komuro I, Wang B, Cheung G, Ishikawa E, Ooboshi H, Bader M, Wada K, Kettenmann H and Noda M, Bradykinin-induced microglial migration mediated by B1-bradykinin receptors depends on Ca2+ influx via reverse-mode activity of the Na+/Ca2+ exchanger. , J Neuroscience, 27(48):13065-73, 2007.11.
26. Eto K, Arimura Y, Nabekura J, Noda M, Ishibashi H., The effect of zinc on glycinergic inhibitory postsynaptic currents in rat spinal dorsal horn neurons., Brain Res., 1161:11-20, 2007.08.
27. Mami Noda, Mizuho A. Kido, Kyota Fujita, Toshihiro Seike, Teruo Tanaka and Haruhiro Higashida, Double-label immunofluorescent staining of CD38 and oxytocin in the mouse hypothalamus. , Nature Protocols, DOI: 10.1038/nprot.2007.166, 2007.05.
28. Noda M, Kariura Y, Pannasch U, Nishikawa K, Wang L, Seike T, Ifuku M, Kosai Y, Wang B, Nolte C, Aoki S, Kettenmann H, Wada K. , Neuroprotective role of bradykinin because of the attenuation of pro-inflammatory cytokine release from activated microglia. , J Neurochem. , 101(2):397-410, 2007.04.
29. Jin D, Liu HX, Hirai H, Torashima T, Nagai T, Lopatina O, Shnayder NA, Yamada K, Noda M, Seike T, Fujita K, Takasawa S, Yokoyama S, Koizumi K, Shiraishi Y, Tanaka S, Hashii M, Yoshihara T, Higashida K, Islam MS, Yamada N, Hayashi K, Noguchi N, Kato I, Okamoto H, Matsushima A, Salmina A, Munesue T, Shimizu N, Mochida S, Asano M, Higashida H. , CD38 is critical for social behavior by regulating oxytocin secretion. , Nature, 446(7131):41-45, 2007.03.
30. Eto K, Arimura Y, Mizuguchi H, Nishikawa M, Noda M, Ishibashi H. , Modulation of ATP-Induced Inward Currents by Docosahexaenoic Acid and Other Fatty Acids in Rat Nodose Ganglion Neurons. J Pharmacol Sci. , J Pharmacol Sci., 102(3):343-346, 2006.11.
31. Sato A, Arimura Y, Manago Y, Nishikawa K, Aoki K, Wada E, Suzuki Y, Osaka H, Setsuie R, Sakurai M, Amano T, Aoki S, Wada K, Noda M., Parkin potentiates ATP-induced currents due to activation of P2X receptors in PC12 cells., J Cell Physiol., 209, 172-182, 2006.10.
32. Manago Y, Kanahori Y, Shimada A, Sato A, Amano T, Sano-Sato Y, Setsuie R, Sakurai M, Aoki S, Wang Y, Osaka H, Wada K and Noda M, Potentiation of ATP-induced currents due to the activation of P2X receptors by ubiquitin carboxy-terminal hydrolase L1., J. Neurochemistry, 10.1111/j.1471-4159.2004.02963.x, 92, 5, 1061-1072, 92, 1061-1072, 2005.03.
33. Noda, M. Kariura, Y., Kosai, Y., Pannasch, U., Wang, L., Kettenmann, H., Nishikawa, K., Okada, S., Aoki, S., Wada, K., Inflammation in the CNS: The role of bradykinin in glial cells., J. Neurochem. Supplement 1, p11 (2004), 88, 11-11, 2004.02.
34. Hagino, Y., Kariura, Y., Manago, Y., Amano, T., Wang, B., Sekiguchi, M., Nishikawa, K., Aoki, S., Wada, K., Noda, M, Heterogeneity and potentiation of AMPA-type of glutamate receptors in rat cultured microglia., GLIA 47: 68-77, 2004, 10.1002/glia.20034, 47, 1, 68-77, 47: 68-77, 2004.05.
35. Noda M., Kariura Y., Amano T., Manago Y., Nishikawa K., Aoki S. and Wada K., Expression and function of bradykinin receptors in microglia., Life Sciences, 72, 1573 ミ 1581 (2003), 10.1016/S0024-3205(02)02449-9, 72, 14, 1573-1581, 72, 1573-1581, 2003.01.
36. Noda, M., Ishihara, T., Kariya, S., Aoki, S., Wada, K., Physiological and molecular biological characterization of M-like channels in glia and neuron., Jpn. J. Physiol., 53, pS86, 2003.01.
37. Noda, M., Yasuda, S., Okada, M., Higashida, H., Nishikawa, K., Aoki, S., Wada, K., Human 5-HT5A receptors and multiple signal transduction pathways., Jpn. J. Physiol., 53, Suppl. pS105, 2003.01.
38. Amano, T., Fujita, A., Sakurai, M., Aoki, A., Wada, K., Noda, M., Electrogenic dopamine transporter in PC12 cells., Jpn. J. Physiol. 53, Suppl. pS200 (2003), 53, Suppl. pS200, 2003.01.
39. Noda M., Yasuda S., Okada M. Higashida H., Shimada A., Iwata N., Ozaki N., Nshikawa K., Shirasawa S., Uchida M., Aoki S., Wada K., Recombinant human 5-HT5A receptors stably expressed in C6 glioma cells couple to multiple signal transduction pathways., J. Neurochemistry, 10.1046/j.1471-4159.2003.01518.x, 84, 2, 222-232, 84, 222-232, 2003.01.
40. Noda, M., Nakanishi, H., Nabekura J. and Akaike, N., AMPA-KA subtypes of glutamate receptor in rat cerebral microglia., J. Neuroscience 20, 251-258 (2000), 20, 1, 251-258, 2000.01.
41. Noda, M.and Nakanishi, H., Discovery of glutamate receptor in rat cerebral microglia., The First Japanese-Korea Joint Symposium., p105-110, 1999.01.
42. Noda M., Nakanishi H. and Akaike N., Glutamate release from microglia via glutamate transporter is enhanced by amyloid-b peptide., Neuroscience, 10.1016/S0306-4522(99)00036-6, 92, 4, 1465-1474, 1999.01.
43. Noda M., Obana M. and Akaike N., Inhibition of M-type K+ current by linopirdine, a neurotransmitter releaase enhancer, in NG108-15 neuronal cells and rat cerebral neurons in culture., Brain Research, 10.1016/S0006-8993(98)00235-2, 794, 2, 274-280, 794, 274-280, 1998.01.
Presentations
1. Mami Noda, Yusaku Yoshioka, Tetsuhi Niiyama, Sex-dependent effects of hypothyroidism in glial morphology and animal behavior, FENS(The Federation of European Neuroscience Societies), 2018.07, Thyroid hormones (THs) are essential for the development and function of the central nervous system (CNS). In the CNS, circulating thyroxine (T4) crosses blood-brain barrier via specific transporters and is taken up to astrocytes, becomes L-tri-iodothyronine (3, 3’, 5–triiodothyronine; T3), an active form of TH, by type 2 de-iodinase (D2). T3 is released to the brain parenchyma from astrocytes (glioendocrine system). In adult CNS, both hypo- and hyper-thyroidism, the prevalence in female being >10 times higher than that in male, may affect psychological condition, for example depression, and potentially increase the risk of cognitive impairment and neurodegeneration including Alzheimer’s disease (AD). We previously reported that non-genomic effects of T3 on microglial functions and its signaling (Mori Y. et al., Glia 63, 906–920, 2015) and sex- and age-dependent effects of THs on glial morphology in the mouse brains of hyperthyroidism (Noda M. Front. Cell. Neurosci. 9:194, 2015; Noda M. et al., OM&P. 2, 85-92, 2016). Here we report that hypothyroidism also induces sex-dependent changes in glial morphology and animal behavior. These results may help to understand physiological and/or pathophysiological functions of THs in the CNS and how hypothyroidism affect behavioral and psychological conditions in sex-dependent manner. Acknowledgement; We appreciate technical help by Research Support Center (Graduate School of Medical Sciences, Kyushu University)..
2. Mami Noda, Kyota Fujita, Margaret A. Hamner, Bruce R. Ransom, PROTECTIVE EFFECTS OF MOLECULAR HYDROGEN AGAINST ISCHEMIC INJURY, 5th European Section meeting of the International Academy of Cardiovascular Sciences (IACS-ES); Advances ın cardıovascular research: from basic mechanisms to therapeutic strategies, 2018.05.
3. Mami Noda., Neuron-glia interaction and sex-dependent animal behaviors in a mouse model of hyperthyroidism., Symposium of Neuro-Glial Interaction, 2018.04.
4. 野田 百美、小林 亜衣, ニコチンはα7アセチルコリン受容体を介してミクログリアのプロトンチャネル活性化を抑制する, 第95回日本生理学会大会, 2018.03.
5. Mami Noda, Miki Yamamoto, Soichi Takiguchi, Mechanism of immune evasion in a mouse model of brain metastasis of lung cancer, 第95回日本生理学会大会, 2018.03.
6. Mami Noda, Possible influence of Orexin in the brain via microglial functional changes., 13th International Symposium on VIP, PACAP, and Related Peptides, 2017.12.
7. Mami Noda, Neuroprotective effects of molecular hydrogen and involvement of stomach-brain interaction, Krasnoyarsk State University Lecture, 2017.11.
8. Mami Noda, Oxidative stress-resistant effects of molecular hydrogen in a mouse model of Parkinson’s disease., "The Molecular Hydrogen 10th Year Anniversary Conference", 2017.09.
9. Mami Noda, Thyroid hormone-regulated neuron-glia interaction in young adult mice and their sex-dependent behavior., MDC seminar, 2017.08.
10. Mami Noda, Neuroprotective and oxidative stress-resistant effects of molecular hydrogen in a mouse model of Parkinson’s disease., University College London (UCL) seminar, 2017.07.
11. Mami Noda, Yusaku Yoshioka, Yosuke Kitahara, Akinori Nishi. , Sex-dependent effect of thyroid hormone in glial-neuronal interaction and animal behavior. , XIII European meeting on glial cells in health and disease. , 2017.07.
12. Mami Noda, Yusuke Yoshii, Taikai Inoue, Yusaku Iwasaki, Toshihiko Yada, Yusaku Nakabeppu. , Complexity of stomach-brain interaction induced by molecular hydrogen in Parkinson’s disease model mice (パーキンソン病モデルマウスにおける分子状水素の複雑な胃―脳連関), 第40回日本神経科学大会(Neuro2017), 2017.07.
13. Mami Noda, Glioendocrine system and neurological dysfunctions., Mediterranean Neuroscience Society 6th Conference 2017, 2017.06.
14. Mami Noda, NEUROPROTECTION BY MOLECULAR HYDROGEN IN PARKINSON’S DISEASE. , VI INTERNATIONAL SYMPOSIUM “INTERACTION OF THE NERVOUS AND IMMUNE SYSTEMS IN HEALTH AND DISEASE”, 2017.06.
15. Mami Noda, Yusaku Yoshioka, Yosuke Kitahara, Akinori Nishi., Thyroid hormone and glioendocrine system in neurological and psychiatric dysfunctions., Cold Spring Harbor Asia - Novel Insights into Glia Function and Dysfunction, 2016.12.
16. Mami Noda, Effects of thyroid hormones in neuron-glia interaction and their sex- and age-dependency., Russian Pathophysiology Society, 2016.12.
17. Mami Noda, Neuroprotective effects of molecular hydrogen and involvement of stomach-brain interaction., A programme of workshop: «The results and perspectives of common investigations of Kyushu University (Fukuoka, Japan) and FSBSI «IEM», Saint-Petersburg, Russia, 2016.12.
18. Jiadai Liu, Satoko Naoe, Taishi Jodoi, Miki Yamamoto, Soichi Takiguchi, Mami Noda. , Interaction between glia cells and lung cancer cells in the progression of brain metastases., Cold Spring Harbor Asia - Novel Insights into Glia Function and Dysfunction, 2016.12.
19. Mami Noda, The latest research trends of hydrogen in Japan - Neuroprotective effects of molecular hydrogen and involvement of stomach-brain interaction., 2016 Korea International Symposium on Hydrogen, 2016.11.
20. Mami Noda, Ai Kobayashi. , Neuroprotective effect of nicotine by inhibition of microglial proton currents via α7 nAChR. , Society for Neuroscience, 46th Annual Meeting., 2016.11.
21. Mami Noda, Yusaku Yoshioka, Yosuke Kitahara, Takahide Shuto, Keisuke Ohta, Kei-ichiro Nakamura, Akinori Nishi, An increase in dendritic spine density in the hippocampus and alterations of sex-dependent animal behaviors in a mouse model of hyperthyroidism. , Society for Neuroscience, 47th Annual Meeting. , 2016.11.
22. MAMI NODA, Ai Kobayashi, Nicotine-induced inhibition of activated microglia and neuroprotection., The 13th Korea-Japan Joint Symposium of Brain Sciences, and Cardiac and Smooth Muscle Sciences, 2016.08.
23. MAMI NODA, Yusaku Yoshioka, Effects of thyroid hormones in neuron-glia interaction., Volga Neuroscience 2016, 2016.07.
24. Mami Noda, Chieri Higashi, Ayaka Fukuo, Jiadai Liu, Neuroprotective effect of molecular hydrogen on ischemic injury in diabetic model mice. , 第39回日本神経科学大会, 2016.07.
25. MAMI NODA, Physiology of microglia., Guangxi University of Chinese Medicine Seminar , 2016.07, [URL].
26. MAMI NODA, Neuroprotective effects of molecular hydrogen; Innovation by a new medical gas, Guangxi University of Chinese Medicine, Seminar in Hospital , 2016.07, [URL].
27. MAMI NODA, Chieri Higashi, Jiadai Liu, Neuroprotective effect of molecular hydrogen in diabetic mouse model., 10th FENS Forum of Neuroscience, 2016.07.
28. MAMI NODA, Glia-endocrine system and neurological disorders., 22nd Scientific Conference, Society on NeuroImmune Pharmacology (SNIP), 2016.04.
29. MAMI NODA, Session 1. Perception, Cognifive, Motor Control and Social Behavior (group discussion), International workshop on “the future of primate neuroscience”., 2016.03.
30. MAMI NODA, Yusuke Yoshii, Taikai Inoue, Multiple Effects of Molecular Hydrogen and its Distinct Mechanism., 6th International Society of Radiation Neurology (ISRN) Conference, 2016.02.
31. MAMI NODA, Possible interaction of thyroid hormones and polyamines in microglia., “Glial Interactions and Brain Experiments” International CaribeGLIA-6 Symposium., 2016.01.
32. MAMI NODA, Jiadai Liu, Yusuke Yoshii, Yusaku Yoshioka, Impact of thyroid hormone on glial function and morphology., Society for Neuroscience, 45th Annual Meeting. , 2015.10.
33. Jiadai Liu, Satoko Naoe, Taishi Jodoi, Soichi Takiguchi, Haruo Iguchi, MAMI NODA, Jiadai Liu, Satoko Naoe, Taishi Jodoi, Soichi Takiguchi, Haruo Iguchi, Mami Noda. Interaction between glia cells and lung cancer cells in microenvironment of brain metastases. (Wuzhen, China, 2015.09.20-23(22)) 6th FAONS: Congress & the 11th Biennial Conference of CNS, 6th FAONS: Congress & the 11th Biennial Conference of CNS, 2015.09.
34. MAMI NODA, Thyroid hormone and glial cells in health and disease. , UOEH (University of Occupational and Environmental Health) Workshop 2015, 2015.09.
35. MAMI NODA, Thyroid dysfunction and glial cells: possible contribution to neurological dysfunctions. , The 3rd Asian Clinical Congress (ACC3) in Tokyo., 2015.09.
36. MAMI NODA, Sex- and age-dependent effect of thyroid hormone on microglia and possible influence on neurodegenerative diseases., The Joint Meeting of the Federation of European Physiological Societies (FEPS) and the Baltic Physiological Societies. , 2015.08.
37. MAMI NODA, Changes in microglial response to glutamate and thyroid hormone in neurodegeneration , 25th ISN (International Society for Neurochemistry) Binneal Meeting., 2015.08.
38. MAMI NODA, Thyroid hormones in glioendocrine system in health and disease., Satellite Meeting in conjunction with the 25th ISN Binneal Meeting – Cairns 2015-, 2015.08.
39. MAMI NODA, Kyota Fujita, Margaret A. Hamner, Yusaku Nakabeppu, Bruce R. Ransom, Protective effects of molecular hydrogen against ischemic injury. In theme “From Basic to Clinical Aspects of Neurology”. , The National Congress of Indonesia Neurological Association VIII and Internationa Symposium, 2015.08.
40. 野田 百美, Mami Noda. Functional change in microglia induced by thyroid dysfunction. Sympoisum (S210a) “Basic and psychological research on microglia” , 第38回日本神経科学大会 (Neuro2015) , 2015.07.
41. MAMI NODA, Microglial dysfunction and neuronal damage in neurodegeneration., International Meeting "Molecular Neurodegeneration - News and Views in Molecular Neuroscience in Health and Disease". , 2015.07.
42. MAMI NODA, Takuma Yoshimura, Liu Jiadai, Yusuke Yoshii, Glioendocrine system of thyroid hormone and its effect on microglia. , XII European Meeting on Glial Cells in Health and Disease (EuroGLIA 2015), 2015.07.
43. MAMI NODA, Jiadai Liu, Yusuke Yoshii, Yusaku Yoshioka, Glioendocrine system and the involvement in neurological dysfunctions. , Cold Spring Harbor Asia - Novel Insights into Glia Function and Dysfunction, 2015.05.
44. MAMI NODA, Taishi Jodoi, Takuma Yoshimura, Soichi Takiguchi, Haruo Iguchi, Glia-tumor interaction in microenvironment of brain metastases. , 第120回日本解剖学会総会・全国学術集会、第92回日本生理学会大会 合同大会, 2015.03.
45. Fumiya Suematsu, Yuichiro Kojima, Haruhiro Higashida, MAMI NODA, Expression and interaction between CD38 and TRPM2 in microglia., 第120回日本解剖学会総会・全国学術集会、第92回日本生理学会大会 合同大会, 2015.03.
46. MAMI NODA, Yuki Mori, Takuma Yoshimura, Liu Jiadai, Yusuke Yoshii, Sex- and age-dependent effects of thyroid hormones on microglial functions. , Gordon Research Conferences-Glial Biology: Functional Interactions Among Glia & Neurons., 2015.03.
47. MAMI NODA, Neuron-glia interaction via thyroid hormone: An example of glioendocrine system. Neuroglia pathology from basic research to clinical practice., グリアの基礎・臨床研究に関するミニシンポジウム, 2015.02.
48. MAMI NODA, Effects of thyroid hormone in microglial function and their signaling. , The 12th Korea-Japan Joint Symposium of Brain Sciences, Cardiac and Smooth Muscle Sciences., 2015.01.
49. MAMI NODA, Yuichiro Kojima, Fumiya Suematsu, Expression of CD38 and its interaction with TRPM2 in microglia. , International Symposium: CD38-NAD Asian 3 countries Meeting Part II, 2014.11.
50. 野田 百美, Kaoru Beppu, Rolf Sprengel, Dysfunction of AMPA-type glutamate receptors in microglia may cause neurodegeneration. (in Symposium “Revealing the prominent role of neuroglia in neurodegeneration” ), Joint Meeting of the Federation of European Phusiological Societies (FEPS) and the Hungarian Physiological Society, 2014.08.
51. MAMI NODA, Possible role of microglial dysfunction in neurodegenative disorders. , INTERNATIONAL CONGRESS ON NEUROSCIENCE , 2014.06.
52. MAMI NODA, Protective effect of new medical gas against Parkinson’s disease. , INTERNATIONAL CONGRESS ON NEUROSCIENCE , 2014.06.
53. MAMI NODA, Protective Role of Microglia and its Mechanism under Stroke: Na+/Ca2+Exchange-Dependent Microglial Migration, (Symposium “Transporters in Glial Cells as New Therapeutic Targets”) , ASPET (American Society for Pharnacology and Experimental Therapeutics) Annual Meeting at Experimental Biology (EB) 2014., 2014.04.
54. MAMI NODA, Akio Matsumoto, Megumi Yamafuji, Tomoko Tachibana, Yusaku Nakabeppu, Haruaki Nakaya, Stomach-brain interaction induced by oral ‘hydrogen water’ in Parkinson’s disease model animal. , Akio Matsumoto, Megumi Yamafuji, Tomoko Tachibana, Yusaku Nakabeppu, Haruaki Nakaya., 2014.04.
55. MAMI NODA, Expression of CD38 in Different Cell Types in the Hypothalamus and Pituitary., 2014 Jeju CD38 and NAD meeting. , 2014.02.
56. MAMI NODA, Functional role for neuropeptides and their signaling cascades in microglial migration (Sympoium: Neuropeptide Signaling in Cellular Interactions: Toward Future Therapeutics), Society for Neuroscience, 43rd Annual Meeting., 2013.11.
57. MAMI NODA, Therapeutic approach to neurodegenerative diseases by medical gases. , FENS Featured Regional Meeting, 2013.09.
58. MAMI NODA, A new target in the treatment for neuropathic pain induced by nerve injury., The 11thKorea-Japan Joint Symposium of Brain Sciences,and Cardiac and Smooth Muscle Sciences , 2013.09.
59. MAMI NODA, Importance of oligodendrocytes in oxidative stress-resistance in white matter ischemic injury., EuroGlia2013, 2013.07.
60. MAMI NODA, CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury., EuroGlia2013, 2013.07.
61. MAMI NODA, Peripheral poly I:C-induced neuroinflammatioin: role of Toll-like receptor 3 (TLR3) in microglia., EuroGlia2013, 2013.07.
62. MAMI NODA, Possible contribution of dysfunction of AMPA-type glutamate receptor in microglia under pathological conditions., eduGLIA, final meeting., 2013.07.
63. MAMI NODA, ROLE OF OLIGODENDROCYTES IN THE PROTECTIVE EFFECTS OF MOLECULAR HYDROGEN AGAINST WHITE MATTER ISCHEMIC INJURY. , ISN (International Society for Neurochemistry, American Society for Neurochemistry) 24th Biennial Joint Meeting, Glial Sattelite , 2013.04.
64. MAMI NODA, Protective effects of molecular hydrogen against ischemic injury, Trans-Pacific Workshop on Stroke 2012. , 2012.10.
65. MAMI NODA, The relationship between CCL-1 and neuron/glia in the neuropathic pain model., Trans-Pacific Workshop on Stroke 2012., 2012.10.
66. MAMI NODA, Plasmalogen attenuate systemic lipopolysaccharide-induced neuroinflammation and β-amyloid protein in adult mice. , Society for Neuroscience, 42nd Annual Meeting, 2012.10.
67. MAMI NODA, Microglia-derived IL-1β is involved in poly I:C-induced fatigue., Society for Neuroscience, 42nd Annual Meeting,, 2012.10.
68. MAMI NODA, The relationship between CCL-1 and neuron/glia in the neuropathic pain model, Society for Neuroscience, 42nd Annual Meeting, 2012.10.
69. MAMI NODA, Bruce R. Ransom, Molecular hydrogen protects against central nervous system white matter ischemic injury., Society for Neuroscience, 42nd Annual Meeting, 2012.10.
70. MAMI NODA, Oral Epithelial Cells are Osmo-sensitive and regulate epithelial barrier via TRPV4. , Society for Neuroscience, 42nd Annual Meeting, 2012.10.
71. MAMI NODA, Role of glial cells in oxidative stress resistance in neurodegenerative diseases., MNS 2012: 4th CONFERENCE OF THE MEDITERRANEAN NEUROSCIENCE SOCIETY, 2012.09.
72. 直江 智子, 山藤 芽実, 藤田 慶大, 毛利 優希, 秋元 望, 上土井 太志, 井口 東郎, 野田 百美, Interaction between glial cells and metastatic lung cancer cells in the brain, Kyushu University-Pusan University Joint Seminar・第11回システム創薬リサーチコア研究会 ・第10回薬学研究院若手研究者セミナー , 2012.09.
73. Mechanism of neuroprotective effects of molecular hydrogen in Parkinson's model mice.
74. Effects of thyroid hormone on microglial function.
75. Mechanism of the effect of thyroid hormone on microglial function.
76. Effects of CCL-1 on neuropathic pain.
77. Interaction between CCL-1 and neuroglia in neuropathic pain.
78. Effects of active form of thyroid hormone on microglial function.
79. Purine2012, [URL].
80. Symposium “Physical Aspect of Medical Science”.
81. Mami Noda1, Satoko Naoe1, Yuki Mohri1, Masataka Ifuku2, Toshihiko Katafuchi, [URL].
82. Effects of thyroid hormone on microglial function.
83. The 10th Japan-Korea Joint Symposium on Brain, Cardiac and Smooth Muscles.
84. Effects of pre-treatment of hydrogen on Parkinson's disease and ischemia model aminals.
85. International Workshop in UOEH 2012.
86. Recovery of oxidative damage by medical gases.
87. The Israel Society for Neuroscience 20th Annual meeting: Israel-Japan Joint Sympoium, [URL].
88. Hydrogen confers resistance to neuronal loss on dopaminergic neurons in mice model of Parkinson’s disease, [URL].
89. Mechanism of inhibition of ATP response in microglia.
90. Effects of thyroid hormone on microglial functions.
91. Bradykinin-, but not ATP- and galanin-induced microglial migration, depends on calcium influx through NCX. , [URL].
92. Neuroprotective effect of hydrogen in Parkinson's disease model mice, [URL].
93. The molecular neurobiology of anti-oxidative stress induced by hydrogen., [URL].
94. Neurotransmitter regulation of microglial motility and phagocytosis.
95. Nicotine inhibits activation of microglial proton currents via interactions with α7 acetylcholine receptors.
96. The relationship between CCL-1 and neuron/glia in the neuropathic pain model..
97. The relationship between CCL-1 and neurons/glial-cells in the neuropathic pain model. , [URL].
98. Relationship between CCL-1 and neuroglia in the development of neuropathic pain.
99. Neuropeptide Receptors in Microglia and their Function..
100. Microenvironment of metastasized tumor cells in the brain. .
101. Neuroprotective effects of hydrogen on MPTP-induced neurotoxicity.
102. Polyriboinosinic : polyribocytidylic acid (PolyI:C)-induced chronic fatigue.
103. Effects of thyroid hormone on microgilal function.
104. Role of GluR2 Subunit of AMPA-type of Glutamate Receptor in Microglia .
105. Brain metastasis of lung cancer and microenvironment in the brain.
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106. Interaction between lung cancer cells and glial cells in brain metastasis..
107. Glutamate receptors in microglia and their loss of function in pathologic conditions. .
108. Activation of microglia is important in polyinosinic-polycytidylic acid (poly I:C)-induced fatigue.
109. Immunologically induced fatigue and glial cells..
110. Role of GluA2 (GluR-B) subunits of AMPA type of glutamate receptor in microglia. .
111. Activation of microglia is important in polyinosinic-polycytidylic acid (poly I:C)-induced fatigue. .
112. Physiological role of GluR2 subunits of AMPA type of Glutamate Receptor in Microglia and pathophysiological implication. .
113. Chemotactic cytokine ligand-1 (CCL-1) contributes to neuropathic pain in mice. .
114. Protective effect of hydrogen on neurodegeneration.
115. Effect of nicotine on proton channel in microglia.
116. Interaction between chemotactic cytokine ligand-1 (CCL-1) and chronic pain.
117. Molecular hydrogen as medical gas; anti-oxidant and ROS-resistant effects in the nervous system..
118. Chemotactic cytokine ligand-1 (CCL-1) contributes to neuropathic pain in mice. .
119. Involvement of glial cells in the development of fatigue.
120. Neuroprotective role of hydrogen on MPTP-induced neurotoxiciy.
121. Gas mediator hydrogen as a tool for protection of Parkinson's disease..
122. Involvement of chemotactic cytokine ligand-1 (CCL-1) in induction of chronic pain and neuron-glia interaction.
123. Hydrogen gas has protective effects on animal model of Parkinson's disease. .
124. Involvement of chemotactic cytokine ligand-1(CCL-1) in neuropathic pain.
125. Effects of hydrogen on Parkinson's disease model animal.
126. Functional role of GluR2 in AMPA-type of glutamate receptor in microglia.
127. Molecular hydrogen as antioxidant: Expectation and improvement of "Medical hydrogen".
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128. Molecular and genetic analyses of neurodegeneration
神経変性疾患の治療薬および予防薬の分子・遺伝子レベルにおける評価法.
129. Function of AMPA-type of glutamate receptors in microglia.
130. Different cellular mechanisms in microglial migration induced by ATP and neuropeptides.
131. Bradykinin-induced incrase in microglial motility and chemotaxisis due to the activation of B1 receptors and Na/Ca exchange system.
132. Oppsite effect of glial cells in the brain metastasis of lung cancer cells.
133. Mechanism of assembling of the brain immune cells to lesion sites.
134. Bradykinin-induced increase in microglial motillity and chemotaxis via Na/Ca exange system.
135. Neuroprotective role of kinin via glial cells in the central nervous system
Mami Noda, Kenjiro Sasaki, Toshihiro Seike, Masataka Ifuku, Bing Wang, Keiji Wada.
136. Bradykinin-induced microglial migration mediated by B1-type of bradykinin receptors depends on Ca2+ influx via reverse mode of Na+/Ca2+ exchanger.
137. Interaction between cancer cells and microenvironment in the brain: the role of astrocytes.
138. The processes of adaptation of microglia in brain trauma and metasitasis..
139. The mechanism of bradykinin B1 receptor-induced microglial migration and chamotaxis.
140. Kinin-induced microglial migration and anti-inflammatory effects in the central nervous system..
141. Protective effects of kinins via microglia in the brain..
142. A possible role of parkin in neurotransmission; potentiation of P2X receptor channels..
143. The role of microglia and astrocytes in brain metastasis of lung-cancer.
144. Bradykinin-induced motility and migration of microglia via B1 receptor.
145. BK-induced migration of microglia.
146. Expression and function of KCNQ channels in microglia.
147. A possible role of parkin and ubiquitin carboxy-terminal hydrolase L1 in neurotransmission; potentiation of P2X receptor channels.
148. The role of microglia in brain metastases: a study using the lung-cancer metastatic model.
149. Effects of parkin and alpha-synuclein on P2X receptor-induced responses.
150. Anti-inflammatory effects of BK in microglia..
151. Characters of KCNQ channels in microglia..
152. Functional importance of Ca2+-activated K+ channels for bradykinin-induced microglial migration..
153. Tricyclic antidepressnat desipramine facilitated glutamate release from presynaptic nerve terminals..
154. Microglia: a sensor for pathology and immune system in the central nervous system..
155. Activation of Ca2+-dependent K+ channels is essential for bradykinin-induced microglial migration.
156. Physiological and molecular biological characterization of KCNQ channels in neuron and glia..
157. Anti-inflammatory effects of kinins via microglia in the central nervous system..
158. Anti-inflammatory effects of kinins in microglia, an immune cell in the central nervous system..
159. Bradykinin-induced microglial motility and its mechanism.
160. AMPA-type of glutamate receptors in microglia..
161. Potentiation of ATP-induced currents due to the activation of P2X receptors by parkin..
162. Potentiation of ATP-induced currents due to the activation of P2X receptors by parkin..
163. Potentiation of ATP-induced currents due to the activation of P2X receptors by parkin..
164. Potentiation of ATP-induced currents due to the activation of P2X receptors by parkin..
165. Membrane translocation of GluR2 and inhibition of glutamate-induced
inward currents in activated microglia.
166. Cyclic ADP ribose coupled to 5-HT receptors in glial cells.
167. Membrane translocation of GluR2 and inhibition of glutamate-induced
inward currents in activated microglia.
168. Membrane translocation of GluR2 and inhibition of glutamate-induced
inward currents in activated microglia.
169. Effects of bradykinin in the brain: the role of microglia.
170. Effects of bradykinin in the brain: the role of microglia.
171. Human 5-HT5A receptors and multiple signal transduction pathways.
172. Electrogenic dopamine transporter in PC12 cells.
173. Regulation of P2X receptor by ubiquitin C-terminal hydrolase 1.
174. Regulation of P2X receptor by ubiquitin C-terminal hydrolase 1.
Membership in Academic Society
  • International Society for hydrogen medicine and biology (ISHMB)
  • International Society for Neurochemistry (ISN)
  • Society for Neuroscience
  • The Japan Neuroscience Society
  • Society for Molecular Hydrogen Medicine and Biology
  • Physiological Society of Japan
  • Brain Science Society
  • The Japanese Society for Neurochemistry
  • Japanese Society of Pathophysiology
  • The Pharmaceutical Society of Japan
  • Women in Physiology of Japan
  • New York Academy of Science
  • The Japanese Pharmacological Society
  • Japanese Cancer Association
Awards
  • Special lecture: Neuroprotective effects of molecular hydrogen; Innovation by a new medical gas
  • Interaction between CCL-1 and neuroglia in neuropathic pain
  • Effects of thyroid hormone on microgial function
Educational
Educational Activities
Classes for undergraduate students:
Physiology and Anatomy
Basic Biopharmacology (in part)
Reading and Writing of Scientific Papers II (in part)

Special course for the graduate students:
Practical Training of Techique of Bio-pharmaceutical Science Experiment
Advanced Research in Clinical Pharmceutics
Other Educational Activities
  • 2017.11, Lecture entitled "Japanese culture and education" at the middle school in Krasnoyarsk (Russia).
  • 2017.11, Lecture entitled "Neuroprotective effects by new medical gas and involvement of stomach-brain interaction" at the School of Pharmacy, Krasnoyarsk State Uniersity, for grade 2 students..
  • 2017.10, Jean-Philippe Rousseau, a PhD student in Laval University, visited for collaboration "Function of thyroid hormone in neuron-glia interaction". The results are presented in Experimental Biology 2018 (San Diego, CA., USA)..
  • 2016.10, Lecture entitled " Charm of the brain science" at Kaho high school Fukuoka Prefecture..
  • 2014.03, A model lecture "Glial research, now and the past" at An Educational Program in the 91st Conference for Physiological Society of Japan (Kagoshima)..
  • 2012.01, Prof. Alexei Verkhratsky comes to our School of Pharmaceutical Sciences as a visiting professor. .
  • 2011.01, Prof. Alexei Verkhratsky came to our School of Pharmaceutical Sciences as a visiting professor..
  • 2011.07, Prof. Alexei Verkhratsky comes to our School of Pharmaceutical Sciences as a visiting professor. .
  • 2011.11, Prof. Bruce Ransom came to our School of Pharmaceutical Sciences as a special lecturer for G30 program. .
  • 2011.09, PhD student, Nozomi Akimoto, went to Max-Delbruck Center, Molecular Medicine, in Berlin, Germany, for about 1 month to collaborate on CCL-1 project..
  • 2011.09, As a mentor in the 54th Japan Neurochemistry annual meeting in Kanazawa, a lecture entitled "How to survive in the major league -Femal version-" was given..
  • 2010.05, I invited Dr. Kristina Zurabovna Shainidze to the 87th Annual meeting of Japanese Physiological Society with their travel grant.
    After that, I invited her to my lab for 1 week. Then I took her to the 12th Brain Science Conference in Kitakyushu to make her presentation..
  • 2010.12, Prof. Bruce Ransom came to our School of Pharmaceutical Sciences as a special lecturer for G30 program..
  • 2009.11, New educational system for graduate students; International Student's Symposium "Kyushu Brain Days".
  • 2007.08.
  • 2006.05.
  • 2005.05.