TRPC5 channel is the mediator of neurotrophin-3 in regulating dendritic growth via CaMKIIalpha in rat hippocampal neurons.

Authors: He, Z  Jia, C  Feng, S  Zhou, K  Tai, Y  Bai, X  Wang, Y 
Citation: He Z, etal., J Neurosci. 2012 Jul 4;32(27):9383-95. doi: 10.1523/JNEUROSCI.6363-11.2012.
Pubmed: (View Article at PubMed) PMID:22764246
DOI: Full-text: DOI:10.1523/JNEUROSCI.6363-11.2012

Neurotrophin-3 (NT-3) plays numerous important roles in the CNS and the elevation of intracellular Ca(2+) ([Ca(2+)](i)) is critical for these functions of NT-3. However, the mechanism by which NT-3 induces [Ca(2+)](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 PLCgamma-dependent [Ca(2+)](i) elevation, which were both blocked when TRPC5, but not TRPC6 channels, were inhibited. Moreover, the Ca(2+) influx through TRPC5 induced by NT-3 inhibited the neuronal dendritic growth through activation of calmodulin-dependent kinase (CaMK) IIalpha. In contrast, the Ca(2+) 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 CaMKIIalpha.


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RGD ID: 10044012
Created: 2015-06-01
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Last Modified: 2015-06-01
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.