TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKII in Rat Hippocampal Neurons

• DOI: 10.1523/jneurosci.6363-11.2012
• Publication Date: 2012-08-01T18:05:51Z
• Authors: Z. He; C. Jia; S. Feng; K. Zhou; Y. Tai; X. Bai; Y. Wang
• Keywords: TRPC5; Colocalization; TRPC6

Neurotrophin-3 (NT-3) plays numerous important roles in the CNS and elevation of intracellular Ca(2+) ([Ca(2+)](i)) is critical for these functions NT-3. However, mechanism by which NT-3 induces [Ca(2+)](i) remains largely unknown. Here, we found that transient receptor potential canonical (TRPC) 5 protein TrkC, receptor, exhibited a similar temporal expression rat hippocampus cellular colocalization hippocampal neurons. Stimulation neurons induced nonselective cation conductance PLCγ-dependent elevation, were both blocked when TRPC5, but not TRPC6 channels, inhibited. Moreover, influx through TRPC5 inhibited neuronal dendritic growth activation calmodulin-dependent kinase (CaMK) IIα. In contrast, NT-4 promoted growth. Thus, acts as novel specific mediator to regulate dendrite development CaMKIIα.