Previous studies indicate that both transient global cerebral ischemia and in vitro ischemic insults can down-regulate the AMPAR subunit GluA2, both at the mRNA and protein levels, in hippocampal neurons [11], [12], [20], [33], [36]–[39], thus inducing a switch from GluA2-containing/Ca2+-impermeable AMPARs to GluA2-lacking/Ca2+-permeable AMPARs. Here, GRIA2 is linked to brain ischemia.