Loss of GluN2A Selectively Impairs Excitatory Synaptic Integration in Hippocampal Somatostatin Interneurons

N-methyl-D-aspartate receptors (NMDARs) are widely considered key determinants of excitatory synaptic kinetics and activity-dependent plasticity, yet their specific contribution to postsynaptic potentials across distinct hippocampal CA1 cell types remains poorly defined. Null variants in GRIN2A are strongly associated with epilepsy-aphasia spectrum disorders, and GluN2A loss has recently been linked to delayed electrophysiological maturation of parvalbumin interneurons, a process regulated by somatostatin interneuron activity. Here, we used Grin2a haploinsufficient and knockout rats to determine how GluN2A depletion affects excitatory synaptic transmission, integration and firing across CA1 pyramidal neurons, parvalbumin interneurons and somatostatin interneurons. Using whole-cell patch-clamp recordings in acute hippocampal slices, we found that NMDARs made no discernible contribution to shaping Schaffer collateral-evoked EPSP kinetics, temporal summation or spike recruitment in CA1 pyramidal neurons at physiological resting potentials. Hebbian long-term potentiation at pyramidal neuron Schaffer collateral synapses was also preserved. Parvalbumin interneuron EPSP kinetics and synaptically evoked firing were similarly unaffected. By contrast, GluN2A loss selectively prolonged EPSP decay in CA1 somatostatin interneurons, increasing EPSP area, enhancing frequency-dependent temporal summation and elevating action potential output during repetitive and theta-frequency synaptic stimulation. These changes occurred alongside an increase in intrinsic excitability, indicating a cell-type-specific alteration by GluN2A loss. Selective enhancement of somatostatin interneuron recruitment provides a candidate mechanism - upstream of delayed parvalbumin interneuron maturation - and may contribute to hippocampal network dysfunction in GRIN2A-related disorders.