Neurotransmitter release is mediated by exocytosis of synaptic vesicles at the presynaptic active zone of nerve terminals. To support rapid and repeated rounds of release, synaptic vesicles undergo a trafficking cycle. The focal point of the vesicle cycle is Ca2+-triggered exocytosis that is followed by different routes of endocytosis and recycling. Recycling then leads to the docking and priming of the vesicles for another round of exo- and endocytosis. Recent studies have led to a better definition than previously available of how Ca2+ triggers exocytosis and how vesicles recycle. In particular, insight into how Munc18-1 collaborates with SNARE proteins in fusion, how the vesicular Ca2+ sensor synaptotagmin 1 triggers fast release, and how the vesicular Rab3 protein regulates release by binding to the active zone proteins RIM1 alpha and RIM2 alpha has advanced our understanding of neurotransmitter release. The present review attempts to relate these molecular data with physiological results in an emerging view of nerve terminals as macromolecular machines.

中文翻译：

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突触小泡循环。

神经递质的释放是由神经末梢突触前活动区的突触小泡的胞吐作用介导的。为了支持快速且反复的释放，突触小泡经历了运输周期。囊泡周期的重点是Ca2 +触发的胞吐作用，随后是胞吞作用和再循环的不同途径。然后，再循环导致囊泡的对接和引发，以进行另一轮胞吐和胞吞作用。最近的研究导致对Ca2 +如何触发胞吐作用以及囊泡如何循环利用的定义比以前更好。特别是，了解Munc18-1如何与SNARE蛋白质协同融合，水泡Ca2 +传感器突触结合素1如何触发快速释放，以及水泡Rab3蛋白如何通过与活性区蛋白RIM1 alpha和RIM2 alpha结合来调节释放，已经使我们对神经递质释放有了更深入的了解。本综述试图将这些分子数据与生理结果联系起来，从而将神经末梢视为一种大分子机器。