Molecular mechanism of synaptic plasticity

突触可塑性的分子机制

• 批准号: 07278103
• 负责人: SHIMIZU Takao
• 金额: $ 143.42万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research on Priority Areas
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-07278103/
• 关键词: lipid mediators; protein kinase C; phospholipases; 血小板活性化因子; プロスタグランジン; ノックアウトマウス; 低分子量Gタンパク; 無脳回症; シグナル伝達; 開口放出; ホスホリパーゼA_2; Miller-Dieker; グリア細胞; プロスタノイド; 神経可塑性; 低分子量Gタンパク質

Various enzymes and receptors for lipid niediators (prostaglandins, leukotrines, platelet-activating factor etc.) have been isolated and their knockout mice were established by the members of this project. By analyzing their phenotypes, it was found that these mediators arc involved in brain functions, synaptogeneses, and neuronal cell development, working in concert with glutamate and other neurotransmitters. we also identified regulations of various types of kinases (protein kinases C, calcium calmodulin-dependent kinases, MAP kinases etc) during synaptic transmission and plasticity. Several small sized GTP binding proteins, and related molecules (SNARE, CREB) are identified of their roles in the synaptic plasticity.

已经分离出了脂质Niediators（前列腺素，白细胞，血小板激活因子等）的各种酶和受体，并由该项目的成员建立了敲除小鼠。通过分析其表型，发现这些介体与脑功能，突触基因因和神经元细胞发育有关，与谷氨酸和其他神经递质一起工作。我们还确定了突触传播和可塑性期间各种类型的激酶（蛋白激酶C，钙钙调蛋白依赖性激酶，MAP激酶等）的法规。几个小尺寸的GTP结合蛋白和相关分子（SNARE，CREB）在突触可塑性中的作用。

项目成果

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