2001 Fiscal Year Final Research Report Summary
Molecular mechanism of synatic vesicle exocytosis-Role of vesicle transport in synaptic plasticity
| Project/Area Number |
10215204
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (B)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokushima Graduate School of Medicine (2000-2001)
Osaka University (1998-1999) |
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Principal Investigator |
SASAKI Takuya The University of Tokushima Graduate School of Medicine, Department of Biochemistry, Professor, 医学研究科, 教授 (40241278)
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| Project Period (FY) |
1998 – 2001
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| Keywords | vesicle transport / neurotransmitter / Rab3A / Doc2 / Rab3 GAP / Rab3 GEP / Rab GDI / Rabconnectin-3 |
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| Research Abstract |
Long-term potentiation (LTP) is believed to provide an important key to understanding the cellular and molecular mechanisms by which memories are formed and stored. Numerous studies strongly suggest that important mechanisms underlying LTP involves alternations in the release of glutamate from the presynaptic cells and the resposiveness of the postsynaptic glutamate receptors. Neurotransmitters including glutamate are released by synaptic vesicle exocytosis which is regulated by many components They are classified into essential and modulatory ones for neurotransmitter release. Rab3A small G protein and Doc2 have been shown to be modulatory components which regulate Ca^<2+>-dependent synaptic vesicle exocytosis. Rab3A cycles between the GDP-bound inactive form and the GTP-bound active form and translocates between the cytosol of the presynaptic nerve terminal and the membranes of synaptic vesicles and the presynaptic plasma membrane. The activation and the translocation are regulated b
… More
y three regulators (Rab GDIα, Rab3 GAP, Rab3 GEP). Our studies on Rab GDIα-deficient mice indicate that this protein is not essential for basal neurotransmitter release but regulates synaptic plasticity. In contrast, Rab3 GEP-deficient mice show much more severe phenotypes and die immediately after birth due to respiratory insufficiency. We isolated a novel protein that was co-immunoprecipitated with Rab3 GEP and GAP by their respective antibodies from the crude synaptic vesicle fraction of rat brain. The protein, named rabconnectin-3, bound at least both Rab3 GEP and GAP. Doc2 interacts with Munc13 in a diacylglycerol-dependent manner, and this interaction is involved in the docking process. Our studies on Doc2-deficient mice indicate that this protein is not essential for basal neurotransmitter release but regulates synaptic plasticity Further studies on the Rab3A and Doc2 systems are necessary for understanding of the molecular mechanism of synaptic plasticity, which may underlie learning and memory Less
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Research Products
(40 results)
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[Publications] Nakanishi, H., et al., Eds. by Nagatsu, T., Nabeshima, R., McCarthy, R., Goldstein, D.: "Rab3A small G protein and its regulators in neurotransmitter release and synaptic plasticity, Catecholamine Research: from Molecular Insights to Clinical Medicine"Kluwer Academic / prenum Publishers. 77-80 (2002)
Description
「研究成果報告書概要(欧文)」より
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