GRIN2B and fragile X syndrome: Eliminating mNMDAR signaling by replacing the GluN2B CTD with the GluN2A CTD phenocopies several core aspects of FXS pathophysiology in the hippocampus, namely, increased density of dendritic spines, an elevated rate of bulk basal protein synthesis, exaggerated LTD mediated by G-protein-coupled metabotropic glutamate receptors (mGluR-LTD) in area CA1, and increased epileptiform activity in area CA3.