Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
MAMI NODA Last modified date:2019.06.21

Associate Professor / Laboratory of Pathophysiology / Department of Pharmaceutical Health Care and Sciences / Faculty of Pharmaceutical Sciences


Papers
1. Liu J, Rybakina EG, Korneva EA, Noda M. , Effects of Derinat on ischemia-reperfusion-induced pressure ulcer mouse model., J Pharmacol Sci. , doi: 10.1016/j.jphs.2018.08.013, 138, 2, 123-130, 2018.10.
2. 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.
3. 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.
4. Wu CY, Hsu WL, Tsai MH, Liang JL, Lu JH, Yen CJ, Yu HS, Noda M, Lu CY, Chen CH, Yan SJ, Yoshioka T., Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress. , Sci Rep., 10.1038/s41598-017-03513-2, 7, 1, 3606, 2017.06, Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca2+ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca2+ signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H2O2. In the present study, H2O2 dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca2+ response, which was partially protected via co-treatment with β-mercaptoethanol, resulting in reduced disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP3Rs). Molecular hydrogen (H2) was found to be more effectively protected H2O2-induced IP3R1 dysfunction by reducing disulfide bonds, rather than quenching ROS. In conclusion, skin aging processes may involve ROS-induced protein dysfunction due to disulfide bond formation, and H2 can protect oxidation of this process..
5. 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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6. Zeidán-Chuliá F, de Oliveira BN, Casanova MF, Casanova EL, Noda M, Salmina AB, Verkhratsky A., Up-regulation of Oligodendrocyte Lineage Markers in the Cerebellum of Autistic Patients: Evidence from Network Analysis of Gene Expression., Molecular Neurobiology , 10.1007/s12035-015-9351-7, 53, 4019-4025, 2016.08.
7. 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..
8. Hsu WL, Lu JH, MAMI NODA, Wu CY, Jia-Dai Liu, Sakakibara M, Tsai MH, Yu HS, Lin MW, Huang YB, Yan SJ, Yoshioka T, Derinat Protects Skin against Ultraviolet-B (UVB)-Induced Cellular Damage.
, Molecules, 10.3390/molecules201119693, 20, 11, 20297-20311, 2015.11.
9. MAMI NODA, Zeidán-Chuliá F, Salmina AB, Verkhratsky A, Rho GTPase RAC1 at the Molecular Interface Between Genetic and Environmental Factors of Autism Spectrum Disorders. , Neuromol Med, 10.1007/s12017-015-8366-6, 2015.08.
10. Zeidán-Chuliá F, de Oliveira BN, Casanova MF, MAMI NODA, Salmina AB, Verkhratsky A, Up-regulation of Oligodendrocyte Lineage Markers in the Cerebellum of Autistic Patients: Evidence from Network Analysis of Gene Expression. , Molecular Neurobiology, 10.1007/s12035-015-9351-7, 2015.08.
11. 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..
12. 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..
13. Zeida´n-Chulia´ F, de Oliveira B-HN, Salmina AB, Casanova MF, Gelain DP, MAMI NODA, Verkhratsky A, Moreira JCF, Altered expression of Alzheimer’s disease-related genes in the cerebellum of autistic patients: a model for disrupted brain connectome and therapy. , Cell Death and Disease , 10.1038/cddis.2014.227, 5, 2014.02.
14. 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.
15. 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..
16. 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..
17. Zeidán-Chuliá F, Rybarczyk-Filho JL, Salmina AB, de Oliveira BH, MAMI NODA, Moreira JC, Exploring the Multifactorial Nature of Autism Through Computational Systems Biology: Calcium and the Rho GTPase RAC1 Under the Spotlight., Neuromolecular Med., 10.1007/s12017-013-8224-3., 15, 2, 364-383, 2013.06, Autism is a neurodevelopmental disorder characterized by impaired social interaction and communication accompanied with repetitive behavioral patterns and unusual stereotyped interests. Autism is considered a highly heterogeneous disorder with diverse putative causes and associated factors giving rise to variable ranges of symptomatology. Incidence seems to be increasing with time, while the underlying pathophysiological mechanisms remain virtually uncharacterized (or unknown). By systematic review of the literature and a systems biology approach, our aims were to examine the multifactorial nature of autism with its broad range of severity, to ascertain the predominant biological processes, cellular components, and molecular functions integral to the disorder, and finally, to elucidate the most central contributions (genetic and/or environmental) in silico. With this goal, we developed an integrative network model for gene-environment interactions (GENVI model) where calcium (Ca(2+)) was shown to be its most relevant node. Moreover, considering the present data from our systems biology approach together with the results from the differential gene expression analysis of cerebellar samples from autistic patients, we believe that RAC1, in particular, and the RHO family of GTPases, in general, could play a critical role in the neuropathological events associated with autism..
18. 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.
19. Terazawa R, Akimoto N, Kato T, Itoh T, Fujita Y, Hamada N, Deguchi T, Iinuma M, MAMI NODA, Nozawa Y, Ito M, A kavalactone derivative inhibits lipopolysaccharide-stimulated iNOS induction and NO production through activation of Nrf2 signaling in BV2 microglial cells. Pharmacol Res., Pharmacol Res., 10.1016/j.phrs.2013.02.002., 71, 34-43, 2013.05, Neuroinflammation and oxidative stress are involved in the pathogenesis of neurodegenerative diseases such as Alzheimer's diseases and Parkinson's disease. Naturally derived kavalactones isolated from Piper methysticum (Piperaceae) have been shown to exhibit neuroprotective effects. We have previously reported that a chemically synthesized kavalactone derivative, 2',6'-dichloro-5-methoxymethyl-5,6-dehydrokawain (compound 1) protects against oxidative stress-induced neuronal cell death through activation of Nrf2 signaling. In the present study, we examined the effect of compound 1 on neuroinflammation. In BV2 microglial cells, compound 1 strongly inhibited LPS-stimulated iNOS induction and NO production, but did not affect LPS-stimulated induction of COX2. At 6h after LPS challenge, when iNOS induction was not clearly seen, treatment with LPS or compound 1 alone increased expression of heme oxygenase 1 (HO-1) whose transcription is regulated by Nrf2. When treated with both, compound 1 enhanced LPS-stimulated HO-1 induction, which was more evident at 24h after LPS treatment. Furthermore, LPS-stimulated activation of Nrf2 signaling and nuclear translocation of Nrf2 were potentiated by compound 1. The mechanism by which compound 1 activated Nrf2 signaling was supposed to be a covalent modification of the sulfhydryl groups of Keap1 by an α,β-unsaturated carbonyl group present in the compound 1. Treatment with hemin, a HO-1 inducer, and with [Ru(CO)₃Cl₂]₂, a CO donor, decreased LPS-stimulated iNOS induction and NO production. In contrast, siRNA-mediated knockdown of HO-1 expression reduced the inhibitory effect of compound 1 on LPS-stimulated iNOS induction and NO production. The compound 1 inhibited LPS-stimulated ERK phosphorylation after LPS treatment. Finally, compound 1 suppressed LPS/IFN-γ-stimulated NO production in primary microglial cells. These results suggest that compound 1 is capable of inhibiting LPS-stimulated iNOS induction and NO production via activation of Nrf2 signaling and HO-1 induction in microglial cells. Taken together, compound 1 has a potential to reduce neuroinflammation as well as oxidative stress in neurodegenerative diseases through activation of Nrf2 signaling..
20. 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..
21. Toshihiko Katafuchi, 井福 正隆, Mawatari S, MAMI NODA, Miake K, Sugiyama M, Fujino T, Effects of plasmalogen on systemic lipopolysaccharide-induced glial activation and -amyloid accumulation in adult mice., Ann. N.Y. Acad. Sci., 10.1111/j.1749-6632.2012.06641.x. , 1262, 85-92, 2012.12.
22. 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.
23. Kei Eto, Hiroaki Wake, Miho Watanabe, Hitoshi Ishibashi, Mami Noda, Yuchio Yanagawa, and Junichi Nabekura , Inter-regional Contribution of Enhanced Activity of the Primary Somatosensory Cortex to the Anterior Cingulate Cortex Accelerates Chronic Pain Behavior
, J. Neurosci., 31, 7631-7636 , 2011.05.
24. 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.
25. 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.
26. Choi J, Ifuku M, Noda M, Guilarte TR, Translocator Protein (18kDa) (TSPO)/Peripheral Benzodiazepine Receptor (PBR) specific ligands induce microglia functions consistent with an activated state., GLIA, Feb;59(2):219-30 (2011), 59, 2, 219-30 , 2011.02.
27. 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.
28. Mami Noda, Effects of neuropeptides in microglia under pathophysiologic conditions. , Eighth Goettingen Meeting of German Neuroscience Society, 2009.03.
29. 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.
30. Yuko Okuno, Masataka Ifuku, Mami Noda, Effects of neuropeptide orexin on microglial migration., Berlin Brain Days; 5th International PhD Symposium, p87, 2008.12.
31. Hiroko Nomaru, K. Kajitani, M. Ifuku, N. Yutsudo, Y. Dan, T. Miura, D. Tsuchimoto, K. Sakumi, T. Kadoya, H. Horie, F. Poirier, M. Noda, Y. Nakabeppu., Galectin-I promotes basal and kainite-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus., Berlin Brain Days; 5th International PhD Symposium, p86, 2008.12.
32. 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.
33. 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.
34. Kido MA, Wang B, Zhang JQ, Kajiya H, Noda M, Yamaza T, Okamoto F, Okabe K. , Charactererization of TARPV1-immunoreactive cells of the palatal rugae in the oral cabvity., Society for Neuroscience, 38th Annual Meeting, 64.23, 2008.11.
35. 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.
36. Katafuchi T., Take S., Ifuku M., Izumi K., Noda M., Yoshimura M., Brain mechanisms of immunologically induced fatigue in the rat , International Conference on Fatigue Science 2008, 2008.09.
37. Mami Noda, Masataka Ifuku, Yukiko Yamakawa, Yuko Okuno, Role of neuropeptide galanin in microglia, 6th FENS Forum , 148.9

, 2008.07.
38. 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.
39. Kajitani K, Nomaru H, Ifuku M, Yutsudo N, Dan Y, Miura T, Tsuchimoto D, Sakumi K, Kadoya T, Horie H, Poirier F, Noda M, Nakabeppu Y, Galectin-1 promotes basal and kainate-induced neurogenesis in the dentate gyrus of adult mouse hippocampus. , Cell Death and Differentiation, 16, 417–427 , 2009.03.
40. 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.
41. 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.
42. 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.
43. 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.
44. 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.
45. 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.
46. Setsuie R, Wang YL, Mochizuki H, Osaka H, Hayakawa H, Ichihara N, Li H, Furuta A, Sano Y, Sun YJ, Kwon J, Kabuta T, Yoshimi K, Aoki S, Mizuno Y, Noda M, Wada K., Dopaminergic neuronal loss in transgenic mice expressing the Parkinson's disease-associated UCH-L1 I93M mutant. , Neurochem Int. , 50(1):119-29, 2007.01.
47. 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.
48. Higashida H, Salmina A, Hashii M, Yokoyama S, Zhang JS, Noda M, Zhong ZG, Jin D. , Bradykinin activates ADP-ribosyl cyclase in neuroblastoma cells: intracellular concentration decrease in NAD and increase in cyclic ADP-ribose. , FEBS Lett., 580(20):4857-4860 , 2006.09.
49. 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.
50. Noda M., Kettenmann H., Wada K., Anti-inflammatory effects of kinins via microglia in the central nervous system., Biol. Chem., 387: 167-171, 2006.02.
51. Sano Y, Furuta A, Setsuie R, Kikuchi H, Wang YL, Sakurai M, Kwon J, Noda M, Wada K., Photoreceptor cell apoptosis in the retinal degeneration of Uchl3-deficient mice., Am J Pathol., 2006.06.
52. Amano T, Aoki S, Setsuie R, Sakurai M, Wada K, Noda M., Identification of a novel regulatory mechanism for norepinephrine transporter activity by the IP(3) receptor., Eur J Pharmacol., 536, 62-8, 2006.02.
53. Ishibashi H, Eto K, Arimura Y, Yamada J, Hatano Y, Nishikawa M, Noda M, Takahama K., Ishibashi H, Eto K, Arimura Y, Yamada J, Hatano Y, Nishikawa M, Noda M, Takahama K. Inhibition of the serotonin-induced inward current by dextromethorphan in rat nodose ganglion neurons. Brain Res. 1097(1):65-70 (2006), Brain Res., 1097(1):65-70, 2006.01.
54. Sakurai M, Ayukawa K, Setsuie R, Nishikawa K, Hara Y, Ohashi H, Nishimoto M, Abe T, Kudo Y, Sekiguchi M, Sato Y, Aoki S, Noda M, Wada K., Ubiquitin C-terminal hydrolase L1 regulates the morphology of neural progenitor cells and modulates their differentiation., J Cell Sci., 119, 162-71, 2006.01.
55. Wang YL, Liu W, Sun YJ, Kwon J, Setsuie R, Osaka H, Noda M, Aoki S, Yoshikawa Y, Wada K., Overexpression of ubiquitin carboxyl-terminal hydrolase L1 arrests spermatogenesis in transgenic mice., Mol Reprod Dev., 73, 40-9, 2006.01.
56. Johansson JU, Lilja L, Chen XL, Higashida H, Meister B, Noda M, Zhong ZG, Yokoyama S, Berggren PO, Bark C., Cyclin-dependent kinase 5 activators p35 and p39 facilitate formation of functional synapses., Brain Res Mol Brain Res., 138, 215-227, 2005.08.
57. 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.
58. Higashida H, Hoshi N, Zhang JS, Yokoyama S, Hashii M, Jin D, Noda M, Robbins J., Protein kinase C bound with A-kinase anchoring protein is involved in muscarinic receptor-activated modulation of M-type KCNQ potassium channels., Neurosci Res., 10.1016/j.neures.2004.11.009, 51, 3, 231-234, 51:231-4, 2005, 2005.01.
59. Ishibashi H, Eto K, Kajiwara M and Noda M., Facilitation of spontaneous glutamate release by antidepressant drugs in rat locus coeruleus., Neurosci Lett, 10.1016/j.neulet.2004.10.045, 374, 2, 152-156, 374 (2), 152-156, 2005.01.
60. Kwon J, Wang Y.L, Setsuie R, Sekiguchi S, Sato Y, Sakurai M, Noda M, Aoki S, Yoshikawa Y and Wada K., Two closely related ubiquitin C-terminal hydrolase isozymes function as reciprocal modulators of germ cell apoptosis in cryptorchid testes., Am. J. Pathol., 10.1016/S0002-9440(10)63394-9, 165, 4, 1367-1374, 165, 1367-1374, 2004.01.
61. Wang YL, Takeda A, Osaka H, Hara Y, Furuta A, Setsuie R, Sun YJ, Kwon J, Sato Y, Sakurai M, Noda M, Yoshikawa Y, Wada K., Accumulation of beta- and gamma-synucleins in the ubiquitin carboxyl-terminal hydrolase L1-deficient gad mouse., Brain Res., 10.1016/j.brainresrev.2004.05.023, 1019, 1-2, 1-9, 1019(1-2):1-9, 2004.09.
62. Kwon J, Wang YL, Setsuie R, Sekiguchi S, Sakurai M, Sato Y, Lee WW, Ishii Y, Kyuwa S, Noda M, Wada K and Yoshikawa Y., Developmental regulation of ubiquitin C-terminal hydrolase isozyme expression during spermatogenesis in mice., Biol. Reprod., 10.1095/biolreprod.104.027565, 71, 2, 515-521, 71(2):515-21, 2004.08.
63. 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.
64. Mari Umezu, Mami Noda, Junicni Nabekura, Hitoshi Ishibashi, Noradrenaline-induced currents in rat airway ganglion neurons., J. Pharmacol. Sci., 94, 190P-190P, 94, Supplement I, 190P, 2004.01.
65. Harada T, Harada C, Wang YL, Osaka H, Amanai K, Tanaka K, Takizawa S, Setsuie R, Sakurai M, Sato Y, Noda M, Wada K., Role of ubiquitin carboxy terminal hydrolase-l1 in neural cell apoptosis induced by ischemic retinal injury in vivo., Am J Pathol., 10.1016/S0002-9440(10)63096-9, 164, 1, 59-64, 164(1):59-64, 2004.01.
66. 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.
67. Misako Kajiwara, Mami Noda, Junichi Nabekura, Hitoshi Ishibashi., Modulation by experimental ischemia of proton-induced currents in rat substantia nigra neurons., J. Pharmacol. Sci. 94, Supplement I, 280P (2004), 94, 280P-280P, 94, Supplement I, 280P, 2004.01.
68. 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.
69. Higashida, H., Mochida, S., Chen, X., Shin, Y., Zhang, J., Hossain, K., Hoshi, N., Hashii, M., Noda, M., Shigemoto, R., Nakanishi, S., Fukuda, Y., Yokoyama, S., Subtype-specific coupling of ADP-rybosyl cyclase of metabotropic glutamate receptors in retina, cervical superior ganglion and NG108-15 cells., Society for Neuroscience, 33rd Annual Meeting, 801.15, 2003.01.
70. 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.
71. 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.
72. 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.
73. 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.
74. Nisikawa K., Li hang, Kawamura R., Osaka H., Wang Y-L., Hara Y., Hirokawa T., Manago Y., Amano, T., Noda, M., Aoki, S., Wada, K., Alterations of structure and hydrolase activity of parkinsonism-associated human ubiquitin carboxyl-terminal hydrolase L1 variants., Biochem Biohys Res Commun, 10.1016/S0006-291X(03)00555-2, 304, 1, 176-183, 304, 176-183, 2003.01.
75. Higashida H, Zhang JS, Mochida S, Chen XL, Shin Y, Noda M, Hossain KZ, Hoshi N, Hashii M, Shigemoto R, Nakanishi S, Fukuda Y, Yokoyama S., Subtype-specific coupling with ADP-ribosyl cyclase of metabotropic glutamate receptors in retina, cervical superior ganglion and NG108-15 cells., J. Neurochemistry, 10.1046/j.1471-4159.2003.01751.x, 85, 5, 1148-1158, 85, 1148-1158, 2003.01.
76. Furuta A, Noda M., Suzuki SO., Goto Y., Kanahori Y., Rothstein JD., Iwaki T., Translocation of glutamate transporter subtype excitatory amino acid carrier 1 protein in kainic acid-induced rat epilepsy., American journal of Pathology, 1, 10.1016/S0002-9440(10)63705-4, 163, 2, 779-787, 163: 779-787, 2003.01.
77. Osaka H., Wang Y-L., Takada K., Takizawa S., Setsuie R., Li H., Sato Y., Nishikawa K., Sun Y-J., Harada T., Hara Y., Kimura I., Chiba S., Namikawa K., Kiyama H., Noda M., Aoki S., Wada K., Ubiquitin carboxy-terminal hydrolase L1 binds to and stabilizes monoubiquitin in neuron., Human Molecular Genetics, 12, 1945-58 (2003), 10.1093/hmg/ddg211, 12, 16, 1945-1958, 12: 945-58, 2003.01.
78. Higashida H., Hossain K. Z., Takahagi H. and Noda M., Measurement of adenylyl cyclase by separating cyclic AMP on silica gel thin-layer chromatography., Analytical Biochemistry, 308, 106-111 (2002), 10.1016/S0003-2697(02)00237-3, 308, 1, 106-111, 2002.01.
79. Higashida H., Yokoyama S., Hoshi N., Hashii M., Egorova A., Zhong Z-G., Noda M., Shahidullah M., Taketo M., Yasuhiro K., Takahashi H., Chen X-L., Shin Y. and Zhang J-S., Signal transduction from brakykinin, angiotensin, adrenergic and muscarinic receptors to effector enzymes, including ADP-ribosyl cyclase., Biological Chemistry, 382,23-30, 2001.01.
80. Higashida H., Hashii M., Yokoyama S., Hoshi N., X-L. Chen X-L., Egorova A., Noda M., and Zhang J-S., Cyclic ADP-ribose as a second messenger revisited from a new aspect of signal transduction from receptors to ADP-ribosyl cyclase., Pharmacology & Therapeutics, 90, 283-296 (2001), 10.1016/S0163-7258(01)00142-5, 90, 2-3, 283-296, 2001.01.
81. Hadley J. K., Noda M., Selyanko,A.A., Wood I. C., Abogadie F. C., Brown D. A., Differential tetraethylammonium sensitivity of KCNQ1-4 potassium channels., Br. J. Pharmacology, 10.1038/sj.bjp.0703086, 129, 3, 413-415, 129(3), 413-415, 2000.01.
82. 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.
83. Noda, M.and Nakanishi, H., Discovery of glutamate receptor in rat cerebral microglia., The First Japanese-Korea Joint Symposium., p105-110, 1999.01.
84. 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.
85. Zhong Z-G., Noda M., Takahashi H. and Higashida H., Overexpression of rat synapsins in NG108-15 neuronal cells enhances functional synapse formation with myotubes., Neuroscience Letters, 260, 93-96 (1999), 1999.01.
86. Higashida H., Egorova A., Higashida C., Zhong Z-G., Yokoyama S., Noda M., Zhang J-S., Sympathetic potentiation of cyclic ADP-ribose formation in rat cardiac myocytes., J. Biological Chemistry, 274, 33348-33354 (1999), 1999.01.
87. Ishizaka N., Noda M., Yokoyama S., Kawasaki K., Yamamoto M. and Higashida H., Muscarinic acetylcholine receptor subtypes in the human iris., Brain Research, 787, 344-347, 1998.01.
88. 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.