Global Grin2a loss causes divergent impairments to PV+ and SST+ interneurons and alters gamma oscillations in prefrontal cortex

GluN2A loss appears to disrupt inhibitory networks through distinct cell-type-specific mechanisms-presynaptic dysfunction in PV⁺ cells and postsynaptic enhancement from SST⁺ cells. PV⁺ dysfunction aligns with gamma synchrony impairments linked to SCZ cognitive flexibility, while SST⁺ alterations may contribute to impaired feedback inhibition and sensory deficits. These findings clarify GluN2A's role in interneuron subtype function and network stability in SCZ.