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首页> 外文期刊>Neuron >Clathrin-mediated endocytosis is the dominant mechanism of vesicle retrieval at hippocampal synapses.
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Clathrin-mediated endocytosis is the dominant mechanism of vesicle retrieval at hippocampal synapses.

机译:网格蛋白介导的内吞作用是海马突触囊泡收回的主要机制。

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摘要

The maintenance of synaptic transmission requires that vesicles be recycled after releasing neurotransmitter. Several modes of retrieval have been proposed to operate at small synaptic terminals of central neurons, including a fast "kiss-and-run" mechanism that releases neurotransmitter through a fusion pore. Using an improved fluorescent reporter comprising pHluorin fused to synaptophysin, we find that only a slow mode of endocytosis (tau = 15 s) operates at hippocampal synapses when vesicle fusion is triggered by a single nerve impulse or short burst. This retrieval mechanism is blocked by overexpression of the C-terminal fragment of AP180 or by knockdown of clathrin using RNAi, and it is associated with the movement of clathrin and vesicle proteins out of the synapse. These results indicate that clathrin-mediated endocytosis is the major, if not exclusive, mechanism of vesicle retrieval after physiological stimuli.
机译:维持突触传递需要释放神经递质后回收囊泡。已经提出了几种在中枢神经元的小突触末端操作的检索模式,包括通过融合孔释放神经递质的快速“吻合”机制。使用包含与突触素融合的pHluorin的改进的荧光报告基因,我们发现当单个神经冲动或短脉冲触发囊泡融合时,海马突触只有慢速内吞作用(tau = 15 s)。该恢复机制被AP180的C端片段的过表达或使用RNAi敲除网格蛋白所阻止,并且与网格蛋白和囊泡蛋白从突触中移动有关。这些结果表明网格蛋白介导的内吞作用是生理刺激后囊泡恢复的主要机制,即使不是唯一的机制。

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