TY - JOUR T1 - TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKIIα in Rat Hippocampal Neurons JF - The Journal of Neuroscience JO - J. Neurosci. SP - 9383 LP - 9395 DO - 10.1523/JNEUROSCI.6363-11.2012 VL - 32 IS - 27 AU - Zhuohao He AU - Caixia Jia AU - Shengjie Feng AU - Kechun Zhou AU - Yilin Tai AU - Xue Bai AU - Yizheng Wang Y1 - 2012/07/04 UR - http://www.jneurosci.org/content/32/27/9383.abstract N2 - Neurotrophin-3 (NT-3) plays numerous important roles in the 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, which were both 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 calmodulin-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. ER -