| Project/Area Number |
15590226
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
TANAKA Hidekazu Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (70273638)
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| Co-Investigator(Kenkyū-buntansha) |
MIKI Naomasa Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (40094445)
KAKU Tetsuki Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (50126570)
TAIRA Eiichi Iwate Medical University Medical School, Professor, 医学部, 教授 (60263240)
IRIE Yasukuki Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (70303948)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | synapse / plasticity / spine / adhesion / cadherin / 可塑性 / 接着分子 |
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| Research Abstract |
Neural activity induces the remodeling of pre- and postsynaptic membranes, which maintain their apposition through cell adhesion molecules. Among them, N-cadherin is redistributed, undergoes activity-dependent conformational changes, and is required for synaptic plasticity. Here we show that depolarization induces the enlargement of the width of spine head, and that cadherin activity is essential for this synaptic rearrangement. Dendritic spines visualized with green fluorescent protein in hippocampal neurons showed an expansion by the activation of AMPA receptor, so that the synaptic apposition zone may be expanded. N-cadherin-venus fusion protein laterally dispersed along the expanding spine head. Overexpression of dominant-negative forms of N-cadherin resulted in the abrogation of the spine expansion. Inhibition of actin polymerization with cytochalasin D abolished the spine expansion. Taken together, our data suggest that cadherin-based adhesion machinery coupled with the actin-cytoskeleton is critical for the remodeling of synaptic apposition zone.
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