Although the aetiology of schizophrenia is still not thoroughly understood, post-mortem studies of patients have consistently revealed alterations of GABAergic interneurons, particularly lower levels of GAD67 and parvalbumin in cortical parvalbumin interneurons (PVs). A deficient maturation of PVs could relate to the neurodevelopmental aspect of schizophrenia since normal wiring of cortical circuits relies on this process. We have previously shown that mice with an early postnatal NMDA receptor ablation in corticolimbic GABAergic interneurons –predominantly PVs– present schizophrenia-like phenotypes that emerge during adulthood. Furthermore, in the medial prefrontal cortex (mPFC), these knockout mice present a functional excitation/inhibition imbalance evident only in the context of increased cortical processing. Here we aimed to further evaluate the cortical microcircuit both functionally and structurally. A greater excitatory drive from the contralateral mPFC was found in fast-spiking interneurons than in pyramidal neurons, regardless of ablation. However, long-range excitatory inputs from the ventral hippocampus failed to show this pattern in the knockout mice. Consequently, in these mice a deficit in feed-forward inhibition was evident at the mPFC by optogenetic stimulation of ventral hippocampus excitatory fibres but not by stimulation of those from the contralateral mPFC. Interestingly, preliminary findings also show a source dependent structural excitatory/inhibitory imbalance, not evident when considering excitatory inputs from contralateral mPFC but manifest when taking into account those from other sources. In conclusion, the early postnatal NMDA receptor ablation from GABAergic interneurons impacts on the development of mPFC microcircuits differentially affecting inputs from homologous transcallosal and long-range sources critical for normal mPFC functioning.