Deletion of TRPC6 Attenuates NMDA Receptor-Mediated Ca Entry and Ca-Induced Neurotoxicity Following Cerebral Ischemia and Oxygen-Glucose Deprivation.

Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na and Ca and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death.