Inhibition of GluN2A NMDA receptors ameliorates synaptic plasticity deficits in the Fmr1 mouse model.

Key Points: Fragile X syndrome (FXS) is a genetic condition that is the most common form of inherited intellectual impairment and causes a range of neurodevelopmental complications including learning disabilities and intellectual disability and shares many characteristics with autism spectrum disorder (ASD). In the FXS mouse model, Fmr1 , impaired synaptic plasticity was restored by pharmacologically inhibiting GluN2A-containing NMDA receptors but not GluN2B-containing receptors. Similar results were obtained by crossing Fmr1 with GluN2A knock-out (Grin2A ) mice.