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进入Ca ²⁺进入，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⁺升高的时空范围，在确定神经信号对突触功能的下游后果中起关键作用。在这里，我们审查了三个主要的细胞内存储的作用：内质网，线粒体和酸性Ca ²⁺存储，如溶酶体，在神经元Ca ²⁺信号传导和可塑性中。我们提供有关Ca如何从这些存储中释放^2+可以调节中央突触的突触前和突触后末端的短期和长期可塑性。