TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity
文献类型：期刊论文
| 作者 | Li, HY ; Huang, JB ; Du, WL ; Jia, CX ; Yao, HL ; Wang, YZ |
| 刊名 | JOURNAL OF NEUROCHEMISTRY
 |
| 出版日期 | 2012 |
| 卷号 | 123期号:6页码:1010-1018 |
| 关键词 | TRAUMATIC BRAIN-INJURY TYROSINE PHOSPHORYLATION GLUCOSE DEPRIVATION CORTICAL CULTURES CEREBRAL-ISCHEMIA CHANNELS MECHANISMS CALCIUM STROKE RATS |
| ISSN号 | 0022-3042 |
| 通讯作者 | 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 |
| 英文摘要 | 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. |
| 学科主题 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
| 收录类别 | SCI |
| 资助信息 | NNSF of China [81130081] |
| 语种 | 英语 |
| 公开日期 | 2013-06-04 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/2509]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | Li, HY,Huang, JB,Du, WL,et al. TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity[J]. JOURNAL OF NEUROCHEMISTRY,2012,123(6):1010-1018. |
| APA | Li, HY,Huang, JB,Du, WL,Jia, CX,Yao, HL,&Wang, YZ.(2012).TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity.JOURNAL OF NEUROCHEMISTRY,123(6),1010-1018. |
| MLA | Li, HY,et al."TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity".JOURNAL OF NEUROCHEMISTRY 123.6(2012):1010-1018. |
入库方式： OAI收割
来源：上海神经科学研究所
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