Myosin Vb介导的突触囊泡转运在突触传递稳态可塑性中的作用及机制

突触传递的稳态可塑性是神经可塑性的重要形式，参与神经系统重要的生理功能及病理过程。在成熟神经元中，突触前和突触后机制共同参与了突触稳态可塑性的建立。目前人们对突触后机制已建立了完善的理论体系，但对突触前机制了解甚少。我们前期实验中发现，突触囊泡的转运参与了稳态可塑性的建立，该过程由负责突触囊泡转运的Myosin Vb介导。进一步研究发现Rbfox1参与了该过程的调控，其通过控制Myosin Vb mRNA的稳定性参与囊泡的转运及突触稳态可塑性的建立。本项目以Myosin Vb作为切入点，研究其表达水平变化对突触囊泡分布和突触传递的影响；进一步探讨Myosin Vb受Rbfox1调控的分子机制，以及Rbfox1在突触传递稳态可塑性中的作用。本项目将研究突触前分子变化在突触传递稳态可塑性中的作用和机制，不仅有助于我们对神经突触可塑性的全面了解，并且为相关精神/神经疾病的研究提供新的思路和靶点。

The homeostatic plasticity of synaptic transmission (homeostatic plasticity of synaptic transmission) is an important form of neuroplasticity, which participates in important physiological functions and pathological processes of the nervous system. In mature neurons, the presynaptic and postsynaptic components jointly participate in the establishment of synaptic homeostasis plasticity. At present, people have established a complete theoretical system for the postsynaptic mechanism, but little is known about the presynaptic mechanism. We found in previous experiments that the mobility of synaptic vesicles is involved in the establishment of homeostatic plasticity, and this process is mediated by the protein Myosin Vb that is responsible for the transport of synaptic vesicles. Further mechanistic studies have found that Rbfox1 is involved in regulating the above process. It participates in the transport of synaptic vesicles and the establishment of synaptic homeostasis plasticity by controlling Myosin Vb mRNA's stability. This project uses Myosin Vb as a research entry point to study its effects on the distribution of synaptic vesicles and synaptic transmission. Further, it explores the molecular mechanism of Myosin Vb regulated by Rbfox1 and the role of Rbfox1 in homeostatic plasticity and synaptic transmission. This project will study the role and mechanism of presynaptic molecular changes in the homeostatic plasticity of synaptic transmission, which will help us fully understand the synaptic plasticity synapses and provide new ideas for the research of related mental/neurological diseases.