Ca²⁺ is an essential trigger for most forms of synaptic plasticity. Ca²⁺ signaling occurs not only by Ca²⁺ entry via plasma membrane channels but also via Ca²⁺ signals generated by intracellular organelles. These organelles, by dynamically regulating the spatial and temporal extent of Ca²⁺ elevations within neurons, play a pivotal role in determining the downstream consequences of neural signaling on synaptic function. Here, we review the role of three major intracellular stores: the endoplasmic reticulum, mitochondria, and acidic Ca²⁺ stores, such as lysosomes, in neuronal Ca²⁺ signaling and plasticity. We provide a comprehensive account of how Ca²⁺ release from these stores regulates short- and long-term plasticity at the pre- and postsynaptic terminals of central synapses.

Ca ²⁺是大多数形式的突触可塑性的重要触发因素。 Ca ²⁺信号传导不仅通过质膜通道的 Ca ²⁺进入发生，而且还通过细胞内细胞器产生的 Ca ²⁺信号发生。这些细胞器通过动态调节神经元内 Ca ²⁺升高的空间和时间范围，在确定神经信号传导对突触功能的下游影响方面发挥着关键作用。在这里，我们回顾了三种主要的细胞内储存：内质网、线粒体和酸性 Ca ²⁺储存（例如溶酶体）在神经元 Ca ²⁺信号传导和可塑性中的作用。我们全面介绍了这些存储中的 Ca ²⁺释放如何调节中央突触突触前和突触后末端的短期和长期可塑性。