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. 2017 Mar 28;11:138. doi: 10.3389/fnins.2017.00138

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Copyright © 2017 Chen, Li, Hatcher, Chen, Chen, Wurster, Chan and Cheng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A schematic drawing to show the role of TRPC6 in I/R- and ODG-induced Ca2+ influx via regulation of NMDARs. TRPC6 expression was increased in neurons following I/R in mice brain and OGD in primary cortical neurons. TRPC6 up-regulation following I/R and OGD induced cortical neuronal death may in part through Na⁺ entry, leading to over-activation of NMDA receptors, and causing an overload of Ca2⁺. Deletion of TRPC6 protects against cerebral ischemia-induced brain damage in vivo and OGD- and excitatory neurotoxin-induced cell death in vitro. This protection is mediated partially through TRPC6-mediated NMDA pathways.