Department of Cell Biology, Howard Hughes Medical Institute and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
Cold Spring Harb Perspect Biol. 2012 Sep 1;4(9):a005645. doi: 10.1101/cshperspect.a005645.
Neurons can sustain high rates of synaptic transmission without exhausting their supply of synaptic vesicles. This property relies on a highly efficient local endocytic recycling of synaptic vesicle membranes, which can be reused for hundreds, possibly thousands, of exo-endocytic cycles. Morphological, physiological, molecular, and genetic studies over the last four decades have provided insight into the membrane traffic reactions that govern this recycling and its regulation. These studies have shown that synaptic vesicle endocytosis capitalizes on fundamental and general endocytic mechanisms but also involves neuron-specific adaptations of such mechanisms. Thus, investigations of these processes have advanced not only the field of synaptic transmission but also, more generally, the field of endocytosis. This article summarizes current information on synaptic vesicle endocytosis with an emphasis on the underlying molecular mechanisms and with a special focus on clathrin-mediated endocytosis, the predominant pathway of synaptic vesicle protein internalization.
神经元在不耗尽其突触小泡供应的情况下可以维持高的突触传递速率。这种特性依赖于突触小泡膜的高效局部内吞循环，它可以重复使用数百次，甚至数千次的外排-内吞循环。在过去的四十年中，形态学、生理学、分子和遗传学研究为控制这种循环及其调节的膜运输反应提供了深入的了解。这些研究表明，突触小泡内吞作用利用了基本和通用的内吞机制，但也涉及到这些机制的神经元特异性适应。因此，对这些过程的研究不仅推动了突触传递领域的发展，而且更广泛地推动了内吞作用领域的发展。本文总结了目前关于突触小泡内吞作用的信息，重点介绍了基础的分子机制，并特别关注网格蛋白介导的内吞作用，这是突触小泡蛋白内化的主要途径。
