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Neurotrophin-3 (NT-3) plays numerous important roles in the central nervous system (CNS) and the elevation of intracellular Ca2+ ([Ca2+]i) is critical for these functions of NT-3.However, the mechanism by which NT-3 induces [Ca2+]i elevation remains largely unknown.Here, we found that transient receptor potential canonical (TRPC) 5 protein and TrkC, the NT-3 receptor, exhibited a similar temporal expression in rat hippocampus and cellular colocalization in hippocampal neurons.Stimulation of the neurons by NT-3 induced a nonselective cation conductance and PLCγ-dependent [Ca2+]i elevation, both were blocked when TRPC5, but not TRPC6 channels,were inhibited.Moreover, the Ca2+ influx through TRPC5 induced by NT-3 inhibited the neuronal dendritic growth through activation of camodulin-dependent kinase (CaMK) Ⅱα.In contrast, the Ca2+ influx through TRPC6 induced by NT-4 promoted the dendritic growth.Thus, TRPC5 acts as a novel and specific mediator for NT-3 to regulate dendrite development through CaMKIIα.