Gan Quan, Watanabe Shigeki
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Front Cell Neurosci. 2018 Jun 28;12:171. doi: 10.3389/fncel.2018.00171. eCollection 2018.
Neurotransmission in complex animals depends on a choir of functionally distinct synapses releasing neurotransmitters in a highly coordinated manner. During synaptic signaling, vesicles fuse with the plasma membrane to release their contents. The rate of vesicle fusion is high and can exceed the rate at which synaptic vesicles can be re-supplied by distant sources. Thus, local compensatory endocytosis is needed to replenish the synaptic vesicle pools. Over the last four decades, various experimental methods and model systems have been used to study the cellular and molecular mechanisms underlying synaptic vesicle cycle. Clathrin-mediated endocytosis is thought to be the predominant mechanism for synaptic vesicle recycling. However, recent studies suggest significant contribution from other modes of endocytosis, including fast compensatory endocytosis, activity-dependent bulk endocytosis, ultrafast endocytosis, as well as kiss-and-run. Currently, it is not clear whether a universal model of vesicle recycling exist for all types of synapses. It is possible that each synapse type employs a particular mode of endocytosis. Alternatively, multiple modes of endocytosis operate at the same synapse, and the synapse toggles between different modes depending on its activity level. Here we compile review and research articles based on well-characterized model systems: frog neuromuscular junctions, neuromuscular junctions, neuromuscular junctions, lamprey reticulospinal giant axons, goldfish retinal ribbon synapses, the calyx of Held, and rodent hippocampal synapses. We will compare these systems in terms of their known modes and kinetics of synaptic vesicle endocytosis, as well as the underlying molecular machineries. We will also provide the future development of this field.
复杂动物中的神经传递依赖于一群功能各异的突触，这些突触以高度协调的方式释放神经递质。在突触信号传递过程中，囊泡与质膜融合以释放其内容物。囊泡融合的速率很高，可能超过远处来源重新供应突触囊泡的速率。因此，需要局部补偿性内吞作用来补充突触囊泡池。在过去的四十年里，人们使用了各种实验方法和模型系统来研究突触囊泡循环的细胞和分子机制。网格蛋白介导的内吞作用被认为是突触囊泡回收的主要机制。然而，最近的研究表明其他内吞模式也有重要作用，包括快速补偿性内吞作用、活动依赖性批量内吞作用、超快内吞作用以及亲吻-逃离。目前尚不清楚是否存在适用于所有类型突触的通用囊泡回收模型。有可能每种突触类型采用特定的内吞模式。或者，多种内吞模式在同一突触中起作用，并且突触根据其活动水平在不同模式之间切换。在这里，我们根据特征明确的模型系统编撰综述和研究文章：青蛙神经肌肉接头、神经肌肉接头、神经肌肉接头、七鳃鳗网状脊髓巨轴突、金鱼视网膜带状突触、Held壶腹以及啮齿动物海马突触。我们将比较这些系统在突触囊泡内吞作用已知模式和动力学方面以及潜在分子机制方面的情况，并展望该领域的未来发展。
