Although GluN2B-containing NMDARs, especially the CTD and phosphorylation of GluN2B, have been suggested to play a role in inducing NMDAR-dependent neurotoxicity, the interaction between GluN2A and metabotropic glutamate receptor 1 (mGluR1) C-terminus seems to be also important for excitotoxicity in a rat model of ischemic stroke (30, 39). This evidence concerns the gene GRM1 and ischemic stroke.