Schematic summary of proposed pathologic changes underlying cerebellar motor dysfunction and autism-like behaviors in CSMD3-deficient mice. CSMD3 deficiency leads to abnormally decreased dendritic complexity but increased immature spine density of cerebellar PCs. Moreover, intrinsic excitability of cerebellar PCs is dramatically increased, and LTD at PF–PC synapses is impaired in the cerebellum of CSMD3^−/− mice. These data suggest that the loss of CSMD3 results in abnormal morphology, increased intrinsic excitabilities, and impaired synaptic plasticity in cerebellar PCs, subsequently leading to motor deficits and autism-like behaviors in mice. GCL, Granular cell layer.