GJD2 and ischemia: In the light of this evidence, we hypothesize that the mechanism of neuroprotection exerted by 2-APB linked with a lower cumulative time of depolarization events can underlie a possible inhibition of Cx36 channels, especially because Cx36 channels are opened by ischemia [64,65] and that the neuroprotection exerted by 2-APB in our study phenocopies the decreased depolarization time observed after ischemia in Cx36-deficient mice [60].