A cell type-specific switch in GluN2D NMDA receptors drives cortical circuit hyperexcitability and sensory-driven cortical synchronization deficits in a Fragile X Syndrome model.
BACKGROUND Altered sensory processing and sensitivity are prevalent in Fragile X Syndrome (FXS) and may be mediated by dysfunction of cortical circuits. Evidence from individuals with FXS and/or the FXS mouse model, Fmr1 KO, indicates hyperexcitability of sensory cortical circuits, deficits in sensory-driven circuit sy...