These data suggest persistent TRPM2 activity following ischemia contributes to impairments of the surviving hippocampal network and that inhibition of TRPM2 channels at chronic time points may represent a novel strategy to improve functional recovery following cerebral ischemia that is independent of neuroprotection.
Activation of transient receptor potential melastatin 2 (TRPM2), an oxidative stress-sensitive Ca<sup>2+</sup>-permeable channel, contributes to the aggravation of cerebral ischemia-reperfusion (CIR) injury.
Corrigendum: The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels.