Schizophrenia is a chronic neurodevelopmental disorder characterized by a complex syndrome that includes psychotic, affective and cognitive features. Our team has previously developed a murine model based on the postnatal ablation of the NR1 subunit of the NMDA receptor in cortical and hippocampal GABAergic interneurons. This approach has proven valuable in reproducing pathophysiological aspects of schizophrenia along with a series of behavioral deficits relevant to its symptomatology. While altered social behaviors have been previously reported in this model, a clear depiction of the affected social domains has not been achieved, precluding the comparison with symptoms of schizophrenia. In this study, we focused on social dominance and aggressive behaviors. In the resident-intruder test, both an increase in the latency to the first attack and a reduction in the number of attacks were detected in knockout animals. Spontaneous dyadic interactions with younger mice and an adaptation of the three-chamber test were also conducted to search for social abnormalities. Determining the face validity of an animal model is crucial to further our understanding of human neuropsychiatric disorders and to develop novel therapeutics.