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

肌球蛋白家族成员是以肌动蛋白为基础的细胞骨架马达，在兴奋性突触的突触可塑性中起着至关重要的作用。在这方面有待研究的两个神经元肌球蛋白是肌球蛋白XVI和肌球蛋白ID。引人注目的是，这些肌球蛋白在物理上与突触可塑性关键调节因子相互作用，似乎与精神疾病有遗传联系。我们假设，肌球蛋白XVI和肌球蛋白ID调节AMPA受体的运输和/或突触后侧的肌动蛋白细胞骨架。我们的目的是验证这一假说，并以小脑浦肯野细胞为模型系统，在体外和体内揭示这些肌球蛋白的功能。我们期望为肌球蛋白依赖的突触可塑性调节机制提供新的线索。

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.