The genetic correlation between synapse formation and memory
| Project/Area Number |
14380374
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | Tokyo Metropolitan Organization for Medical Research |
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Principal Investigator |
SAITOE Minoru Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, Chief of staff scientists, 東京都神経科学総合研究所, 主任研究員 (50261839)
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| Co-Investigator(Kenkyū-buntansha) |
MIYASHITA Tomoyuki Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, Staff scientist, 東京都神経科学総合研究所, 研究員 (70270668)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2003: ¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 2002: ¥7,100,000 (Direct Cost: ¥7,100,000)
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| Keywords | Drosophila / syntaxin / synapse formation / spontaneous vesicle release / syntaxin(syx) / syntaxin / cAMP / CaMKII / Gene Chip |
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| Research Abstract |
The syntaxin (syx) gene encodes a synaptic plasma membrane protein that regulates synaptic vesicle release in association with synaptic vesicle protein such as synaptotagmin and synaptobrevin. In syx mutants, spontaneous vesicle release is absent, and postsynaptic receptor clusters are scarcely formed. We have hypothesized that synaptic vesicle contains clustering agent, and spontaneous vesicle release is sufficient to induce postsynaptic receptor clusters. In order to examine the role of spontaneous vesicle exocytosis more precisely, we analyze the developmental changes of synapse function and morphology in syx mutant embryos. At the early stage of synapse formation, we found spontaneous vesicle release in a quite low frequency manner suggesting contribution of maternal Syx protein. In consistent with this finding, synaptic receptor clusters were rarely observed. However, the ratio of the receptor cluster to synaptic area and intensity of clusters were significantly reduced in syx mutants. Furthermore, we found presynaptic defects in syx mutants. Number of synaptic branches were decreased, synaptic boutons swelled and less developed. These results suggest that maternal Syx protein contributes to residual spontaneous vesicle release at the early stage of synapse formation and Leads to rarely observed receptor clusters. syx regulates development of presynaptic terminals as well as synaptic vesicle release.
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Report
(3 results)
Research Products
(6 results)
