Schizophrenia is a severe neurodevelopmental disorder characterized by positive and negative symptoms as well as cognitive impairment, which drastically hinders self-sufficiency. Thus, understanding the underlying circuits related to cognitive deficits is crucial. In mice, cognition correlates with synchronous activity in the mPFC, maintained by reciprocal synapses between pyramidal neurons (PNs) and interneurons, particularly parvalbumin interneurons (PVIs). We used a mouse model of PVI dysfunction in which NMDARs are eliminated in corticolimbic interneurons, predominantly PVIs, which displays cognitive deficits and mPFC circuit alterations, including excitation/inhibition (E/I) imbalance in PNs. We hypothesized that mPFC circuit alterations in KO mice could be attributed to a deficit in PVI-PN synaptic maturation, hence we performed an immunohistochemical quantification of pre and postsynaptic perisomatic markers in PNs. These structural results reveal differences between developmental stages and suggest a disbalanced expression of both GABAAR α1 and α2 subunits in adult KO mice, without changes in PV puncta density. Furthermore, in an additional experiment we performed a correlation analysis between PVI/GABAARα1 perisomatic puncta and miniature EPSCs and IPSCs electrophysiologically recorded in the same PN. These structural-functional results suggest adult KO mice lack a homeostatic compensatory mechanism for maintaining an appropriate E/I balance.