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网格蛋白介导的突触末端内吞作用:连接生理学和分子之间的桥梁。

Clathrin-mediated endocytosis at the synaptic terminal: bridging the gap between physiology and molecules.

机构信息

Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Crown Street, Liverpool L69 3BX, UK.

出版信息

Traffic. 2010 Dec;11(12):1489-97. doi: 10.1111/j.1600-0854.2010.01104.x.

DOI:10.1111/j.1600-0854.2010.01104.x
PMID:20633242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3371399/
Abstract

It has long been known that the maintenance of fast communication between neurons requires that presynaptic terminals recycle the small vesicles from which neurotransmitter is released. But the mechanisms that retrieve vesicles from the cell surface are still not understood. Although we have a wealth of information about the molecular details of endocytosis in non-neuronal cells, it is clear that endocytosis at the synapse is faster and regulated in distinct ways. A satisfying understanding of these processes will require molecular events to be manipulated while observing endocytosis in living synapses. Here, we review recent work that seeks to bridge the gap between physiology and molecules to unravel the endocytic machinery operating at the synaptic terminal.

摘要

长期以来,人们一直认为神经元之间保持快速通讯需要突触前末梢从释放神经递质的小泡中循环利用。但是,从细胞表面回收小泡的机制仍未被理解。尽管我们已经获得了大量关于非神经元细胞胞吞作用分子细节的信息,但很明显,突触处的胞吞作用更快,并且以不同的方式进行调节。要想令人满意地理解这些过程,需要在观察活突触内胞吞作用的同时对分子事件进行操作。在这里,我们回顾了最近的一些研究工作,这些工作旨在弥合生理学和分子学之间的差距,以揭示在突触末端起作用的胞吞作用机制。

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本文引用的文献

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Activity-dependent bulk endocytosis and clathrin-dependent endocytosis replenish specific synaptic vesicle pools in central nerve terminals.活动依赖性胞吞作用和网格蛋白依赖性胞吞作用补充中枢神经末梢特定的突触小泡池。
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Dynamin I phosphorylation by GSK3 controls activity-dependent bulk endocytosis of synaptic vesicles.GSK3 介导的动力蛋白 I 磷酸化控制突触囊泡的活性依赖的批量内吞作用。
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AP-1/sigma1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory.AP-1/σ1B-衔接蛋白介导内体突触囊泡循环、学习和记忆。
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Endocytosis and clathrin-uncoating defects at synapses of auxilin knockout mice.auxilin 敲除小鼠突触处的胞吞作用和网格蛋白解包被缺陷。
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