Bidirectional regulation of Ca2+ in exo-endocytosis coupling
Bidirectional regulation of Ca2+ in exo-endocytosis coupling
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Ca2 在胞吐-内吞耦合中的双向调节
DOI：
10.1007/s11427-018-9429-6
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Changhe Wang
中科院分区：
文献类型：
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作者：
Qian Song;Mingzhu Huang;Bianbian Wang;Xinjiang Kang;Changhe Wang
囊泡胞吐是神经递质释放的关键过程，而囊泡再循环对于质膜结构的稳态和神经传递的维持至关重要。Ca 2+调节几种基本的细胞过程（Zhu等人，2016; Xiong and Zhu，2016）。特别是Ca 2+内流在神经元和内分泌细胞中具有触发囊泡胞吐和调节代偿性胞吞的双重作用。囊泡胞吐作用通过Ca 2+依赖性或Ca 2+非依赖性机制发生（Chai等人，2017），并且质膜下的局部Ca 2+信号在胞吐作用的融合孔扩张和融合模式（完全融合对吻和跑）的确定中起关键作用（Wang等人，2017年）。Ca 2+在外吞-内吞过程中的正性和负性作用均有报道，但Ca 2+在外吞-内吞偶联过程中的确切作用仍有争议。虽然钙调素和突触连接蛋白1（Syt 1）是促进内吞作用的主要Ca 2+感受器，但内吞过程中Ca 2+抑制的分子机制尚不清楚。本文着重介绍了神经传递过程中Ca 2+在胞吞作用中的作用及其机制.
Vesicular exocytosis is a key process involved in neurotransmitter release, whereas vesicle recycling is critical for the homeostasis of plasma membrane structures and the maintenance of neurotransmission. Ca 2+ regulates several fundamental cellular processes (Zhu et al., 2016; Xiong and Zhu, 2016). Especially, Ca 2+ influx plays a dual role of triggering vesicular exocytosis and modulating compensatory endocytosis in neurons and endocrine cells. Vesicular exocytosis occurs either by Ca 2+-dependent or Ca 2+-independent mechanisms (Chai et al., 2017), and local Ca 2+ signals beneath the plasma membrane plays a critical role in the determination of the fusion pore dilation and fusion modes (full fusion vs. kiss-and-run) of exocytosis (Wang et al., 2017). Both positive and negative roles of Ca 2+ in exo–endocytosis have been reported; however, the exact role of Ca 2+ in exo–endocytosis coupling remains debatable. Although calmodulin and synaptotamgin-1 (Syt1) function as primary Ca 2+ sensors that promote endocytosis, the molecular mechanism of Ca 2+ inhibition in endocytosis remains unknown. The present article focuses on the role and underlying mechanisms of Ca 2+ in endocytosis during neurotransmission.