| Project/Area Number |
08457591
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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 |
Physical pharmacy
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KIRINO Yutaka Professor, School of Pharmaceutical Sciences, The University of Tokyo, 大学院・薬学系研究所, 教授 (10012668)
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| Co-Investigator(Kenkyū-buntansha) |
HIRASHIMA Naohide Research Associate, The University of Tokyo School of Pharmaceutical Sciences, 大学院・薬学系研究所, 助手 (10192296)
SUZUKI Toshiharu Associate Professor, The University of Tokyo School of Pharmaceutical Sciences, 大学院・薬学系研究所, 助教授 (80179233)
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| Project Period (FY) |
1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1996: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | Acetylcholine / Presynaptic terminals / Electric Ray / Electric organ / Adenosine receptors / Ca channels / Lambert-Eaton syndrome / 神経前終末 / アセチルコリン遊離 / アデノシン / リン脂質非対称分布 |
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| Research Abstract |
(1)There exist N-, P/Q- and L-type voltage-dependent Ca channels (VDCCs) in the presynaptic plasma membranes of nerve terminals of the electric organ isolated from the Japanese electric ray Narke japonica. The acetylcholine (ACh) release was predominantly mediated by-and P/Q-type VDCCs. (2)cDNA for synaphine was cloned from the cDNA library prepared from the electric lobe of the ray. Synaphine was found to be associated with syntaxin, VAMP and SNAP-25, suggesting its involvement in the exocytosis. (3)cDNA for the Alzheimer's beta-amyolid presursor protein (APP) was also isolated from the above cDNA library. The analysis indicated the product protein, APP,was phosphorylated after its maturation. (4)There exist adenosine A_1 and A_<2B> receptors in the electric organ synaptic membrane. Activation of the latter increses the ACh release via potentiation of P/Q-type VDCCs while the activation of the former reduces the ACh release via inhibition of N-type VDCCs. (5)Antibodies from the lambert-Eaton syndrome (LES) patients reduced the ACh release by its specific down-regulation of P/Q-type VDCCs. (6)Immunization of rats or mice with the electric organ synaptosomes produced an animal model of LES.
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