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Title: TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity
Author: Li, HY ; Huang, JB ; Du, WL ; Jia, CX ; Yao, HL ; Wang, YZ
Source: JOURNAL OF NEUROCHEMISTRY
Issued Date: 2012
Volume: 123, Issue:6, Pages:1010-1018
Keyword: TRAUMATIC BRAIN-INJURY ; TYROSINE PHOSPHORYLATION ; GLUCOSE DEPRIVATION ; CORTICAL CULTURES ; CEREBRAL-ISCHEMIA ; CHANNELS ; MECHANISMS ; CALCIUM ; STROKE ; RATS
Subject: Biochemistry & Molecular Biology ; Neurosciences & Neurology
Corresponding Author: Wang, YZ (reprint author), Chinese Acad Sci, Lab Neural Signal Transduct, Inst Neurosci, SIBS,State Key Lab Neurosci, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.,yzwang@ion.ac.cn
English Abstract: Excitotoxicity induced by NMDA receptor-mediated intracellular Ca2+ ([Ca2+]i) overload is a major cause of delayed neuronal death in cerebral ischemia. Transient receptor potential canonical (TRPC) 6 protects neurons from ischemic brain damage. However, the mechanisms by which TRPC6 protects neurons are largely unknown. Here, we reported that TRPC6 suppressed the [Ca2+]i elevation induced by NMDA and protected neurons from excitotoxicity. Over-expressing or down-regulating TRPC6 suppressed or aggravated Ca2+ overload under excitotoxicity, respectively. TRPC6 protected cultured neurons from damage caused by NMDA toxicity or oxygen glucose deprivation (OGD). Moreover, the infarct volume in TRPC6 transgenic (Tg) mice was smaller than that in wild-type (WT) littermates. The TRPC6 Tg mice had better behavior performance and lower mortality than their WT littermates. Thus, TRPC6 inhibited NMDA receptor-triggered neurotoxicity and protected neurons from ischemic brain damage. Increase in TRPC6 activity could be a potential strategy for stroke prevention and therapy.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/2509
Appears in Collections:神经所(总)_期刊论文

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Li, HY; Huang, JB; Du, WL; Jia, CX; Yao, HL; Wang, YZ.TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity,JOURNAL OF NEUROCHEMISTRY,2012,123(6):1010-1018
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