We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
TRPC6 inhibited NMDA receptor activities and protected neurons from ischemic excitotoxicity.
- Authors
Li, Hongyu; Huang, Junbo; Du, Wanlu; Jia, Caixia; Yao, Hailan; Wang, Yizheng
- 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.
- Subjects
TRP channels; METHYL aspartate receptors; CEREBRAL ischemia; CELL death; BRAIN damage; TRANSGENIC mice
- Publication
Journal of Neurochemistry, 2012, Vol 123, Issue 6, p1010
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/jnc.12045