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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-/y , impaired synaptic plasticity was restored by pharmacologically inhibiting GluN2A-containing NMDA receptors but not GluN2B-containing receptors. Similar results were obtained by crossing Fmr1-/y with GluN2A knock-out (Grin2A-/- ) mice. These results suggest that dampening the elevated levels of GluN2A-containing NMDA receptors in Fmr1-/y mice has the potential to restore hyperexcitability of the neural circuitry to (a more) normal-like level of brain activity.
Pubmed ID: 30132892 RIS Download
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