Hosoi Nobutake, Holt Matthew, Sakaba Takeshi
Independent Junior Research Group of Biophysics of Synaptic Transmission, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Neuron. 2009 Jul 30;63(2):216-29. doi: 10.1016/j.neuron.2009.06.010.
The mechanism coupling exocytosis and endocytosis remains to be elucidated at central synapses. Here, we show that the mechanism linking these two processes is dependent on microdomain-Ca2+ similar to that which triggers exocytosis, as well as the exocytotic protein synaptobrevin/VAMP. Furthermore, block of endocytosis has a limited, retrograde action on exocytosis, delaying recruitment of release-ready vesicles and enhancing short-term depression. This effect sets in so rapidly that it cannot be explained by the nonavailability of recycled vesicles. Rather, we postulate that perturbation of a step linking exocytosis and endocytosis temporarily prevents new vesicles from docking at specialized sites for exocytosis.
在中枢突触中，耦合胞吐作用和胞吞作用的机制仍有待阐明。在此，我们表明连接这两个过程的机制依赖于微区[Ca2+]（i），类似于触发胞吐作用的[Ca2+]（i），以及胞吐蛋白突触囊泡蛋白/囊泡相关膜蛋白（VAMP）。此外，胞吞作用的阻断对胞吐作用具有有限的逆行作用，延迟了释放准备好的囊泡的募集并增强了短期抑制。这种效应起效非常迅速，无法用再循环囊泡的不可用性来解释。相反，我们推测胞吐作用和胞吞作用之间一个步骤的扰动暂时阻止了新的囊泡停靠在用于胞吐作用的特化位点。
