Mechanisms of Actomyosin-Dependent Regulation of Postsynaptic Function and Plasticity in Purkinje Cells

肌动蛋白为基础的细胞骨架马达的肌球蛋白家族的成员在兴奋性突触的突触可塑性中起着至关重要的作用。两个神经元肌球蛋白，仍然是在这方面的特点是肌球蛋白XVI和肌球蛋白Id。引人注目的是，这些肌球蛋白物理相互作用的突触可塑性的关键监管机构，似乎是遗传相关的精神疾病。我们假设肌球蛋白XVI和肌球蛋白Id调节AMPA受体运输和/或肌动蛋白细胞骨架在突触后侧。我们的目的是测试这一假设，并揭示这些肌球蛋白在体外和体内使用小脑浦肯野细胞作为模型系统的功能。我们希望能对肌球蛋白依赖的突触可塑性调节机制有新的认识。

Members of the myosin family of actin-based cytoskeletal motors play crucial roles for synaptic plasticity at excitatory synapses. Two neuronal myosins that remain to be characterized in this respect are myosin XVI and myosin Id. Strikingly, these myosins physically interact with synaptic plasticity key regulators and appear to be genetically associated with psychiatric disorders. We hypothesize that myosin XVI and myosin Id regulate AMPA receptor trafficking and/or the actin cytoskeleton at the postsynaptic side. Our aim is to test this hypothesis and to uncover the function of these myosins in vitro and in vivo using cerebellar Purkinje cells as a model system. We expect to shed new light on the mechanisms of myosin-dependent synaptic plasticity regulation.