Updated on 2022/03/31

写真a

 
SUGIO Shouta
 
Organization
Graduate School of Medicine Center for Research of Laboratory Animals and Medical Research Engineering Division for Advanced Medical Research Assistant Professor
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Assistant Professor

Degree 1

  1. 博士(理学) ( 2013.9   総合研究大学院大学 ) 

Research Interests 1

  1. Glial cell, Myelin

Research Areas 1

  1. Life Science / Neuroscience-general  / グリア細胞、髄鞘

Research History 4

  1. Nagoya University   Graduate School of Medicine   Assistant Professor

    2020.4

  2. Kobe University   Graduate School of Medicine   Assistant Professor

    2018.10 - 2020.3

  3. Kobe University   Graduate School of Medicine

    2018.4 - 2018.9

  4. Gunma University   Graduate School of Medicine   Researcher

    2015.4 - 2018.3

Education 1

  1. The Graduate University for Advanced Studies

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    Country: Japan

Professional Memberships 3

  1. THE PHYSIOLOGICAL SOCIETY OF JAPAN

  2. THE JAPANESE SOCIETY FOR NEUROCHEMISTRY

  3. THE JAPAN NEUROSCIENCE SOCIETY

 

Papers 10

  1. Ca<sup>2+</sup> imaging with two-photon microscopy to detect the disruption of brain function in mice administered neonicotinoid insecticides.

    Hirai A, Sugio S, Nimako C, Nakayama SMM, Kato K, Takahashi K, Arizono K, Hirano T, Hoshi N, Fujioka K, Taira K, Ishizuka M, Wake H, Ikenaka Y

    Scientific reports   Vol. 12 ( 1 ) page: 5114   2022.3

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    Language:English  

    DOI: 10.1038/s41598-022-09038-7

    PubMed

  2. Elucidation of the neurological effects of clothianidin exposure at the no-observed-adverse-effect level (NOAEL) using two-photon microscopy in vivo imaging.

    Nishi M, Sugio S, Hirano T, Kato D, Wake H, Shoda A, Murata M, Ikenaka Y, Tabuchi Y, Mantani Y, Yokoyama T, Hoshi N

    The Journal of veterinary medical science     2022.3

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    Language:English  

    DOI: 10.1292/jvms.22-0013

    PubMed

  3. Detection of brain function disruption caused by nicotinic acetylcholine receptor agonists using Ca<sup>2+</sup> imaging with two-photon microscopy

    HIRAI Anri, SUGIO Shouta, NIMAKO Collins, NAKAYAMA Shouta M.M., KATO Keisuke, TAKAHASHI Keisuke, ARIZONO Koji, HIRANO Tetsushi, HOSHI Nobuhiko, FUJIOKA Kazutoshi, TAIRA Kumiko, ISHIZUKA Mayumi, WAKE Hiroaki, IKENAKA Yoshinori

    Annual Meeting of the Japanese Society of Toxicology   Vol. 48.1 ( 0 ) page: P-37E   2021

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    Language:Japanese   Publisher:The Japanese Society of Toxicology  

    <p>Neonicotionoid pesticides are insecticides which have been thought to be one of the causes of Colony Collapse Disorder. They were considered to be less toxic to mammals than insects, but some of the recent studies suggested their association with disruption of higher brain fuction in mammals. Nevertheless, it is still unclear how neonicotionoids affect on the central nervous system. Here, we propose the use of in vivo Ca<sup>2+</sup> imaging with two-photon microscope to detect abnormal activity of neuronal circuits in brain with the application of neonicotionoids.</p><p>In this study, a less than the no-observed-adverse-effect level (NOAEL) of acetamiprid (20 mg/kg bw); and a tenth or half of the median lethal doses of nicotine (0.33 or 1.65 mg/kg bw respectively) were orally administered to mice. They were subjected to elevated plus maze test and Ca<sup>2+</sup> imaging by two-photon microscope in the somatosensory cortex. We further detected acetamiprid and metabolites in brain and blood an hour after the administration.</p><p>Mice exposed to acetamiprid or nicotine exhibited an increase in anxiety-like behavior that associated with the altered activities of the neuronal population in the somatosensory cortex. Although the dose of acetamiprid used in the current study was below the NOAEL, both acetamiprid and nicotine affected the behavior and the neuronal activity in the somatosensory cortex. The results suggested that in vivo Ca<sup>2+</sup> imaging using two-photon microscope enabled highly sensitive detection of brain neurodisruption by neurotoxicants.</p>

    DOI: 10.14869/toxpt.48.1.0_p-37e

    CiNii Research

  4. Maternal immune activation induces sustained changes in fetal microglia motility

    Ozaki Kana, Kato Daisuke, Ikegami Ako, Hashimoto Akari, Sugio Shouta, Guo Zhongtian, Shibushita Midori, Tatematsu Tsuyako, Haruwaka Koichiro, Moorhouse Andrew J., Yamada Hideto, Wake Hiroaki

    SCIENTIFIC REPORTS   Vol. 10 ( 1 ) page: 21378   2020.12

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  5. Motor learning requires myelination to reduce asynchrony and spontaneity in neural activity. Reviewed International journal

    Daisuke Kato, Hiroaki Wake, Philip R Lee, Yoshihisa Tachibana, Riho Ono, Shouta Sugio, Yukio Tsuji, Yasuyo H Tanaka, Yasuhiro R Tanaka, Yoshito Masamizu, Riichiro Hira, Andrew J Moorhouse, Nobuaki Tamamaki, Kazuhiro Ikenaka, Noriyuki Matsukawa, R Douglas Fields, Junichi Nabekura, Masanori Matsuzaki

    Glia   Vol. 68 ( 1 ) page: 193 - 210   2020.1

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    Publishing type:Research paper (scientific journal)  

    Myelination increases the conduction velocity in long-range axons and is prerequisite for many brain functions. Impaired myelin regulation or impairment of myelin itself is frequently associated with deficits in learning and cognition in neurological and psychiatric disorders. However, it has not been revealed what perturbation of neural activity induced by myelin impairment causes learning deficits. Here, we measured neural activity in the motor cortex during motor learning in transgenic mice with a subtle impairment of their myelin. This deficit in myelin impaired motor learning, and was accompanied by a decrease in the amplitude of movement-related activity and an increase in the frequency of spontaneous activity. Thalamocortical axons showed variability in axonal conduction with a large spread in the timing of postsynaptic cortical responses. Repetitive pairing of forelimb movements with optogenetic stimulation of thalamocortical axon terminals restored motor learning. Thus, myelin regulation helps to maintain the synchrony of cortical spike-time arrivals through long-range axons, facilitating the propagation of the information required for learning. Our results revealed the pathological neuronal circuit activity with impaired myelin and suggest the possibility that pairing of noninvasive brain stimulation with relevant behaviors may ameliorate cognitive and behavioral abnormalities in diseases with impaired myelination.

    DOI: 10.1002/glia.23713

    Scopus

    PubMed

  6. The dynamics of revascularization after white matter infarction monitored in Flt1-tdsRed and Flk1-GFP mice. Reviewed International journal

    Hiroya Shimauchi-Ohtaki, Masashi Kurachi, Masae Naruse, Koji Shibasaki, Shouta Sugio, Ken Matsumoto, Masatsugu Ema, Yuhei Yoshimoto, Yasuki Ishizaki

    Neuroscience letters   Vol. 692   page: 70 - 76   2019.1

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    Publishing type:Research paper (scientific journal)  

    Subcortical white matter infarction causes ischemic demyelination and loss of brain functions, as the result of disturbances of the blood flow. Although angiogenesis is one of the recovery processes after cerebral infarction, the dynamics of revascularization after white matter infarction still remains unclear. We induced white matter infarction in the internal capsule of Flk1-GFP::Flt1-tdsRed double transgenic mice by injection of endothelin-1 (ET-1), a vasoconstrictor peptide, together with N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and followed the changes in Flk1 and Flt1 expression in the vascular system in the infarct area. Reduction of Flt1-tdsRed-positive blood vessels 1 day after the injection and increase of Flk1-GFP-strongly-positive blood vessels 3 days after the injection were apparent. PDGFRβ-strongly-positive (PDGFRβ+) cells appeared in the infarct area 3 days after the injection and increased their number thereafter. Three days after the injection, most of these cells were in close contact with Flk1-GFP-positive endothelial cells, indicating these cells are bona fide pericytes. Seven days after the injection, the number of PDGFRβ+ cells increased dramatically, and the vast majority of these cells were not in close contact with Flk1-GFP-positive endothelial cells. Taken together, our results suggest revascularization begins early after the ischemic insult, and the emerging pericytes first ensheath blood vessels and then produce fibroblast-like cells not directly associated with blood vessels.

    DOI: 10.1016/j.neulet.2018.10.057

    PubMed

  7. Ectopic positioning of Bergmann glia and impaired cerebellar wiring in Mlc1-over-expressing mice. Reviewed

    Kikuchihara S, Sugio S, Tanaka KF, Watanabe T, Kano M, Yamazaki Y, Watanabe M, Ikenaka K

    Journal of neurochemistry   Vol. 147 ( 3 ) page: 344 - 360   2018.11

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  8. Retinal Detachment-Induced Müller Glial Cell Swelling Activates TRPV4 Ion Channels and Triggers Photoreceptor Death at Body Temperature. Reviewed International journal

    Hidetaka Matsumoto, Shouta Sugio, François Seghers, David Krizaj, Hideo Akiyama, Yasuki Ishizaki, Philippe Gailly, Koji Shibasaki

    The Journal of neuroscience : the official journal of the Society for Neuroscience   Vol. 38 ( 41 ) page: 8745 - 8758   2018.10

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    Using region-specific injection of hyaluronic acid, we developed a mouse model of acute retinal detachment (RD) to investigate molecular mechanisms of photoreceptor cell death triggered by RD. We focused on the transient receptor potential vanilloid 4 (TRPV4) ion channel, which functions as a thermosensor, osmosensor, and/or mechanosensor. After RD, the number of apoptotic photoreceptors was reduced by ∼50% in TRPV4KO mice relative to wild-type mice, indicating the possible involvement of TRPV4 activation in RD-induced photoreceptor cell death. Furthermore, TRPV4 expressed in Müller glial cells can be activated by mechanical stimuli caused by RD-induced swelling of these cells, resulting in release of the cytokine MCP-1, which is reported as a mediator of Müller glia-derived strong mediator for RD-induced photoreceptor death. We also found that the TRPV4 activation by the Müller glial swelling was potentiated by body temperature. Together, our results suggest that RD adversely impacts photoreceptor viability via TRPV4-dependent cytokine release from Müller glial cells and that TRPV4 is part of a novel molecular pathway that could exacerbate the effects of hypoxia on photoreceptor survival after RD.SIGNIFICANCE STATEMENT Identification of the mechanisms of photoreceptor death in retinal detachment is required for establishment of therapeutic targets for preventing loss of visual acuity. In this study, we found that TRPV4 expressed in Müller glial cells can be activated by mechanical stimuli caused by RD-induced swelling of these cells, resulting in release of the cytokine MCP-1, which is reported as a mediator of Müller glia-derived strong mediator for RD-induced photoreceptor death. We also found that the TRPV4 activation by the Müller glial swelling was potentiated by body temperature. Hence, TRPV4 inhibition could suppress cell death in RD pathological conditions and suggests that TRPV4 in Müller glial cells might be a novel therapeutic target for preventing photoreceptor cell death after RD.

    DOI: 10.1523/JNEUROSCI.0897-18.2018

    PubMed

  9. Transient receptor potential vanilloid 2 activation by focal mechanical stimulation requires interaction with the actin cytoskeleton and enhances growth cone motility Reviewed

    Shouta Sugio, Masami Nagasawa, Itaru Kojima, Yasuki Ishizaki, Koji Shibasaki

    FASEB JOURNAL   Vol. 31 ( 4 ) page: 1368 - 1381   2017.4

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    Authorship:Lead author   Publishing type:Research paper (scientific journal)   Publisher:FEDERATION AMER SOC EXP BIOL  

    We have previously reported that transient receptor potential vanilloid 2 (TRPV2) can be activated by mechanical stimulation, which enhances axonal outgrowth in developing neurons; however, the molecular mechanisms that govern the contribution of TRPV2 activation to axonal outgrowth remain unclear. In the present study, we examined thismechanismby using PC12 cells as a neuronalmodel. Overexpression of TRPV2 enhanced axonal outgrowth in a mechanical stimulus-dependent manner. Accumulation of TRPV2 at the cell surface was 4-fold greater in the growth cone compared with the soma. In the growth cone, TRPV2 is not static, but dynamically accumulates (within similar to 100ms) to the site ofmechanical stimulation. The dynamic and acute clustering ofTRPV2 can enhance very weak mechanical stimuli via focal accumulation of TRPV2. Focal application of mechanical stimuli dramatically increasedgrowth conemotility andcausedactin reorganization via activationofTRPV2. Wealso found that TRPV2 physically interacts with actin and that changes in the actin cytoskeleton are required for its activation. Here, we demonstrated for the first time to our knowledge that TRPV2 clustering is induced by mechanical stimulation generated by axonal outgrowth and that TRPV2 activation is triggered by actin rearrangements that result frommechanical stimulation. Moreover, TRPV2activationenhances growthcone motility andactinaccumulationto promote axonal outgrowth. Sugio, S., Nagasawa, M., Kojima, I., Ishizaki, Y., Shibasaki, K. Transient receptor potential vanilloid 2 activation by focal mechanical stimulation requires interaction with the actin cytoskeleton and enhances growth cone motility.

    DOI: 10.1096/fj.201600686RR

    Web of Science

    PubMed

  10. Astrocyte-Mediated Infantile-Onset Leukoencephalopathy Mouse Model Reviewed

    Shouta Sugio, Koujiro Tohyama, Shinichiro Oku, Kanehiro Fujiyoshi, Takeshi Yoshimura, Keigo Hikishima, Ryutaro Yano, Takahiro Fukuda, Masaya Nakamura, Hideyuki Okano, Masahiko Watanabe, Masaki Fukata, Kazuhiro Ikenaka, Kenji F. Tanaka

    GLIA   Vol. 65 ( 1 ) page: 150 - 168   2017.1

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    Authorship:Lead author   Publishing type:Research paper (scientific journal)   Publisher:WILEY-BLACKWELL  

    Astrocytes have recently been shown to provide physiological support for various brain functions, although little is known about their involvement in white matter integrity. Several inherited infantile-onset leukoencephalopathies, such as Alexander disease and megalencephalic leukoencephalopathy with subcortical cysts (MLC), implicate astrocytic involvement in the formation of white matter. Several mouse models of MLC had been generated by knocking out the Mlc1 gene; however, none of those models was reported to show myelin abnormalities prior to formation of the myelin sheath. Here we generated a new Mlc1 knockout mouse and a Mlc1 overexpressing mouse, and demonstrate that astrocyte-specific Mlc1 overexpression causes infantile-onset abnormalities of the white matter in which astrocytic swelling followed by myelin membrane splitting are present, whereas knocking out Mlc1 does not, and only shows myelin abnormalities after 12 months of age. Biochemical analyses demonstrated that MLC1 interacts with the Na+/K+ ATPase and that overexpression of Mlc1 results in decreased activity of the astrocytic Na+/K+ pump. In contrast, no changes in Na+/K+ pump activity were observed in Mlc1 KO mice, suggesting that the reduction in Na+/K+ pump activity resulting from Mlc1 overexpression causes astrocytic swelling. Our infantile-onset leukoencephalopathy model based on Mlc1 overexpression may provide an opportunity to further explore the roles of astrocytes in white matter development and structural integrity. We established a novel mouse model for infantile-onset leukoencephalopathy by the overexpression of Mlc1. Mlc1 overexpression reduced activity of the astrocytic sodium pump, which may underlie white matter edema followed by myelin membrane splitting.

    DOI: 10.1002/glia.23084

    Web of Science

    PubMed

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MISC 4

  1. 行動毒性試験および二光子イメージングによるアセタミプリドの神経毒性評価

    平井杏梨, 杉尾翔太, 池中良徳, COLLINS Nimako, 中山翔太, 星信彦, 和氣弘明, 石塚真由美

    日本獣医学会学術集会講演要旨集   Vol. 163rd   2020

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  2. 剥離網膜におけるミュラー細胞浮腫と炎症の関係

    松本英孝, 柴崎貢志, 杉尾翔太, 石崎泰樹, 秋山英雄

    日本眼科学会雑誌   Vol. 122 ( 臨増 ) page: 294 - 294   2018.3

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    Language:Japanese  

    J-GLOBAL

  3. 剥離網膜におけるミュラー細胞TRPV4活性化とATP放出

    松本英孝, 柴崎貢志, 杉尾翔太, 石崎泰樹, 秋山英雄

    日本眼科学会雑誌   Vol. 121 ( 臨増 ) page: 219 - 219   2017.3

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    Language:Japanese  

    J-GLOBAL

  4. 小脳登上線維‐プルキンエ細胞間シナプスの精緻化へのグリア細胞の関与

    菊地原沙織, 菊地原沙織, 杉尾翔太, 杉尾翔太, 稲村直子, 稲村直子, 渡辺雅彦, 田中謙二, 渡邉貴樹, 狩野方伸, 山崎良彦, 池中一裕, 池中一裕

    日本生理学雑誌(Web)   Vol. 79 ( 1 ) page: WEB ONLY   2017.2

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    Language:Japanese  

    J-GLOBAL

KAKENHI (Grants-in-Aid for Scientific Research) 3

  1. Developmental neurotoxicity of pesticides based on the transgenerational inheritance and localized neural progenitor and glial cells activity

    Grant number:21K19846  2021.7 - 2024.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

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    Authorship:Coinvestigator(s) 

  2. Analysis of molecular and cellular basis of activity-dependent myelination

    Grant number:19K21211  2019.4 - 2020.3

    SUGIO SHOUTA

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    Authorship:Principal investigator 

    Grant amount:\2990000 ( Direct Cost: \2300000 、 Indirect Cost:\690000 )

    Our brain is composed from neurons and glial cells. Recent studies have unveiled that oligodendrocytes (OCs), a type of glial cells, extend numerous processes to neuronal axons and communicate together to regulate neuronal conduction velocity, which likely mediated by processes of OCs. Here, we performed two-photon microscopy in vivo and patch clamp recording in acute brain slice using a transgenic mouse that expressed a fluorescent calcium indicator (GCaMP6) in OCs.Two-photon imaging revealed that an oligodendrocyte has various spaciotemporal pattern of calcium activity at each processes within a cells, and we demonstrated that changes in neuronal activity are affected to the calcium responses of oligodendtocytes. Notably, the frequency and active spots are increased with neuronal activation and decreased with neuronal suppression. Moreover, patchclamp analysis indicated that the calcium transient in oligodendrocyte is mediated by neurotransmitters.

  3. 神経活動依存性髄鞘形成の分子基盤の解明:脳白質は可塑的であるか?

    2018.10 - 2020.3

    文部科学省  科学研究費補助金 (研究活動スタート支援) 

    杉尾 翔太

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    Authorship:Principal investigator  Grant type:Competitive

 

Teaching Experience (On-campus) 1

  1. 解剖学実習(頭頚部、神経解剖)

    2020