Neurotrophin-3 (NT-3), a member of neurotrophin family, exerts numerous functions in central nerves system regarding for its ability to induce intracellular calcium elevation, however, the identity of calcium channel and mechanism involved in its actions remains largely unknown.Here, we found that the temporal expression and cellular localization pattern of Transient receptor potential canonical (TRPC) 5 protein paralleled that of NT-3 receptor TrkC in hippocampal neurons.Activation by NT-3 led to production of nonselective cation conductance and PLCγ-dependent intracellular calcium elevation, which was reduced after blockade of TRPC5 but not TRPC6 channels in hippocampal neurons.Moreover, the specific calcium influx through TRPC5 induced by NT-3 inhibited hippocampus neuronal dendritic growth through Camodulin-dependent Kinase (CaMK) Ⅱ activation, whereas the calcium influx through TRPC6 induced by NT-4 promoted hippocampus neuronal dendritic growth through CaMKIV activation.Thus TRPC channels emerge as novel and specific mediators of neurotrophin-regulated dendritic development through specific CaMKs.