Neuronal signal integration, synaptic transmission and plasticity highly depend on the morphology of dendrites. Here, we found that neuronal Nogo-A, which was known so far as a myelin associated protein inhibiting neurite outgrowth, influences dendrite morphology and synaptic transmission in the cerebellum. Synaptic strength between parallel fibers and Purkinje dendrites was reduced due to the postsynaptic overexpression of Nogo-A in Purkinje cells. Overexpression of Nogo-A in Purkinje cells reduced the volume and complexity of the dendritic arborization, whereas deletion of Nogo-A induced larger than normal dendritic tree. Patch clamp recordings of Purkinje cells in acute slices showed increased spontaneous firing and excitability of Nogo-A overexpressing Purkinje cells. This increase can be fully explained by the decreased cell size and a reduced dendritic arborization that lead to a decrease in cell capacitance. In contrast, Purkinje cells of Nogo-A KO mice show a significant decreased excitability cell size caused by their increased size. Spine width was negatively regulated by Nogo-A. Microarray analysis of laser captured Purkinje neurons overexpressing Nogo-A revealed the upregulation of the small GTPase signaling pathway as well as their downstream effectors actin and tubulin mRNAs. Thus, cytoskeletal rearrangements in the dendrites may be responsible for the observed changes in synaptic transmission. This study demonstrates that neuronal Nogo-A may play a critical role in the regulation of dendrite morphogenesis and neurotransmission at the cerebellar level.