This study suggested that our EA pretreatment regime could effectively increase the neurofunction and reduce the volume of cerebral infarction and the level of neuronal apoptosis in the hippocampal CA1 region for an animal model of cerebral I/R injury, and its mechanism may be related to the inhibition of the GluN2B/m-calpain/p38 MAPK proapoptotic pathway. Here, GRIN2B is linked to brain infarction.