The concentration of calcium ions in presynaptic terminals regulates transmitter release, but underlying mechanisms have remained unclear. Here we review recent studies that shed new light on this issue. Fast-freezing electron microscopy and total internal reflection fluorescence microscopy studies reveal complex calcium-dependent vesicle movements including docking on a millisecond time scale. Recordings from so-called ‘simple synapses’ indicate that calcium not only triggers exocytosis, but also modifies synaptic strength by controlling a final, rapid vesicle maturation step before release. Molecular studies identify several calcium-sensitive domains on Munc13 and on synaptotagmin-1 that are likely involved in bringing the vesicular and plasma membranes closer together in response to calcium elevation. Together, these results suggest that calcium-dependent vesicle docking occurs in a wide range of time domains and plays a crucial role in several phenomena including synaptic facilitation, post-tetanic potentiation, and neuromodulator-induced potentiation.

突触前末梢钙离子浓度调节递质释放，但潜在机制仍不清楚。在这里，我们回顾了最近的研究，这些研究为这个问题提供了新的思路。快速冷冻电子显微镜和全内反射荧光显微镜研究揭示了复杂的钙依赖性囊泡运动，包括在毫秒时间尺度上的对接。来自所谓的“简单突触”的记录表明，钙不仅触发胞吐作用，而且通过控制释放前最终的、快速的囊泡成熟步骤来改变突触强度。分子研究确定了 Munc13 和突触结合蛋白-1 上的几个钙敏感结构域，它们可能参与使囊泡和质膜更靠近以响应钙升高。一起，