Modulation of excitation on parvalbumin interneurons by neuroligin-3 regulates the hippocampal network

The authors show that postsynaptic deletion of neuroligin-3 from parvalbumin interneurons causes a decrease in NMDA-receptor-mediated excitatory postsynaptic currents and an increase in presynaptic glutamate release probability linked to a deficit in presynaptic Group III metabotropic glutamate receptor function. This selective disruption of excitatory transmission on parvalbumin interneurons leads to abnormal hippocampal network activity and a decrease in contextual fear extinction.