| Project/Area Number |
21500346
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Niigata University |
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Principal Investigator |
ABE Teruo 新潟大学, 脳研究所, 非常勤講師 (50010103)
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| Co-Investigator(Renkei-kenkyūsha) |
YAO Hiromu 東北大学, 大学院・生命科学研究科, 教授 (00144353)
YAMADA Mitsunori 独立行政法人国立病院機構, さいがた病院・検査部, 部長 (30240039)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経伝達物質放出 / 可溶性タンパク質 / シナプス小胞 / ノックアウト |
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| Research Abstract |
To understand the mechanisms by which soluble proteins such as Munc18-1, tomosyn 1 and synaphin/complexin regulate synaptic vesicle exocytosis, we generated hippocampal CA3-specific knockout(KO) mice of Munc18-1 and tomosyn 1. Neuronal degeneration was already apparent 1week after birth in mice lacking the Munc18-1 gene in the CA3 region, rendering the analysis of synaptic transmission difficult. Tomosyn 1 KO mice exhibited larger EPSPs and smaller paired pulse facilitations. The involvement of the binding of the synaphin C-terminal region with synaptotagmin 1 in dense-core vesicle exocytosis from PC12 cessl was suggested.
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