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Title: TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKII alpha in Rat Hippocampal Neurons
Author: He, ZH ; Jia, CX ; Feng, SJ ; Zhou, KC ; Tai, YL ; Bai, X ; Wang, YZ
Source: JOURNAL OF NEUROSCIENCE
Issued Date: 2012
Volume: 32, Issue:27, Pages:9383-9395
Keyword: PROTEIN-KINASE-II ; PHOSPHATIDYLINOSITOL 4 ; 5-BISPHOSPHATE ; SIGNAL-TRANSDUCTION ; INTRACELLULAR CA2+ ; CALCIUM REGULATION ; PYRAMIDAL NEURONS ; TRK RECEPTORS ; BDNF ; TRANSCRIPTION ; CELLS
Subject: Neurosciences & Neurology
Corresponding Author: Wang, YZ (reprint author), 320 Yueyang Rd, Shanghai 200031, Peoples R China.,yzwang@ion.ac.cn
English Abstract: 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 PLC gamma-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) II alpha. 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 CaMKII alpha.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/2508
Appears in Collections:神经所(总)_期刊论文

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He, ZH; Jia, CX; Feng, SJ; Zhou, KC; Tai, YL; Bai, X; Wang, YZ.TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKII alpha in Rat Hippocampal Neurons,JOURNAL OF NEUROSCIENCE,2012,32(27):9383-9395
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