突触小泡胞吐作用的分子机制。
The molecular machinery of synaptic vesicle exocytosis.
作者信息
Li L, Chin L-S
机构信息
Department of Pharmacology, Center for Neurodegenerative Disease, Emory University School of Medicine, 1510 Clifton Road, Atlanta, Georgia 30322-3090, USA.
出版信息
Cell Mol Life Sci. 2003 May;60(5):942-60. doi: 10.1007/s00018-003-2240-7.
At the synapse, neurotransmitters are released via Ca(2+)-triggered exocytotic fusion of synaptic vesicles with the presynaptic plasma membrane. Synaptic vesicle exocytosis seems to share many basic principles and homologous proteins with other membrane fusion events. Conserved components of the general fusion machinery that participate in synaptic vesicle exocytosis include soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), ATPase N-ethylmaleimide-sensitive factor, Munc18/nSec1, Rab3 GTPase, and the exocyst proteins. In addition, synaptic vesicle exocytosis uses a set of unique components, such as synaptotagmin, complexin, Munc13, and RIM, to meet the special needs of fast Ca(2+)-triggered neurotransmitter release. This review summarizes present knowledge about the molecular mechanisms by which these components mediate and/or regulate synaptic vesicle exocytosis.
在突触处，神经递质通过Ca(2+)触发的突触小泡与突触前质膜的胞吐融合而释放。突触小泡胞吐似乎与其他膜融合事件共享许多基本原理和同源蛋白。参与突触小泡胞吐的一般融合机制的保守成分包括可溶性N-乙基马来酰亚胺敏感因子附着蛋白受体（SNAREs）、ATP酶N-乙基马来酰亚胺敏感因子、Munc18/nSec1、Rab3 GTP酶和外被蛋白复合体。此外，突触小泡胞吐利用一组独特的成分，如突触结合蛋白、结合素、Munc13和RIM，来满足快速Ca(2+)触发的神经递质释放的特殊需求。本综述总结了关于这些成分介导和/或调节突触小泡胞吐的分子机制的现有知识。
Zotero 插件