2017 Fiscal Year Final Research Report
Studies on communication between neuroaxons via oligodendrocytes.
Project Area | Glial assembly: a new regulatory machinery of brain function and disorders |
Project/Area Number |
25117005
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Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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Allocation Type | Single-year Grants |
Review Section |
Biological Sciences
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Research Institution | National Institute for Physiological Sciences |
Principal Investigator |
Ikenaka Kazuhiro 生理学研究所, 分子細胞生理研究領域, 教授 (00144527)
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Co-Investigator(Kenkyū-buntansha) |
山崎 良彦 山形大学, 医学部, 准教授 (10361247)
田中 謙二 慶應義塾大学, 医学部(信濃町), 准教授 (30329700)
清水 健史 名古屋市立大学, 医学部, 講師 (60398237)
小林 憲太 生理学研究所, 行動・代謝分子解析センター, 准教授 (70315662)
畑中 伸彦 生理学研究所, システム脳科学研究領域, 助教 (80296053)
吉村 武 生理学研究所, 分子細胞生理研究領域, 助教 (60402567)
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Project Period (FY) |
2013-06-28 – 2018-03-31
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Keywords | グリア / 精神疾患 / 神経興奮制御 / 活動電位の伝達速度 |
Outline of Final Research Achievements |
Oligodendrocytes (OLs) have recently been shown to modulate conduction velocity in an axonal activity-dependent manner even after myelination is completed. The axonal activity also promotes the proliferation and differentiation of OL precursor cells, and these are required for motor skill learning. Taken together, these findings suggest that neuronal activity and subsequent myelin remodeling are required for executing higher brain function. We thus examined whether and/or how OLs play roles in higher brain functions, using following experimental systems. (1) A method for simultaneously labeling both axons from different brain regions and the myelinating OL, (2) Mouse lines with channelrhodopsin-2 expression in OL, (3) NF155 conditional knockout mice, whose paranodes are disrupted after their initial formation.
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Free Research Field |
神経生物学
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