突触传递是神经细胞互相传递信息最主要的手段，是大脑发挥其正常功能的重要基础。关于突触传递机制的研究是神经科学中最基础，最核心的重要研究内容。突触传递受突触前活动区蛋白紧密调控，具体的分子调控机制还很不清楚。CAST/ELKS是突触前活动区核心蛋白之一，但是关于CAST/ELKS在突触传递中的具体作用还有争议，特别是在哺乳动物中的作用还很不清楚。本项目提出假说：CAST/ELKS通过调节突触前膜上电压依赖性钙通道数量以及突触释放可能性来调节突触传递及可塑性。为此，本项目以小鼠Calyx of Held突触为研究模型，采用电生理，电子显微镜，免疫组织化学等技术手段，对CAST/ELKS在突触传递和可塑性中的调节作用进行详细的研究，并阐明其机制，为进一步理解突触传递可塑性的分子机制打下基础。

Synaptic transmission is the most important way neurons used to communicate with each other, is critical for normal brain function. The study of mechanisms of synaptic transmission is the most basic, core research field of neuroscience research. synaptic transmission is tightly regulated by presynaptic active zone proteins, and the underlying mechanisms are still not fully understood. This project makes the hypothesis: CAST/ELKS regulate synaptic transmission and plasticity through regulating the number of voltage-gated calcium channels and synaptic release probability. To test this hypothesis, we use Calyx of Held synapse as a model, employ electrophysiology, electromicroscopy and IHC to study the role and underlying mechanisms of CAST/ELKS on synaptic transmission and plasticity. It will provide more mechanism insights into the regulation of synaptic transmission and plasticity.