“…Other genetic models have found that deleting the GluN1 subunit of the NMDAR, either constitutively, in corticolimbic inhibitory neurons, in parvalbumin inhibitory neurons, or in forebrain pyramidal neurons leads to cognitive, social, and electrophysiological (i.e., gamma band oscillations) changes reminiscent of schizophrenia (Belforte et al, 2009; Jadi, Margarita Behrens, & Sejnowski, 2015; Tatard-Leitman et al, 2015). Mice lacking the protein dybsindin, (an original candidate risk gene), which is reduced in schizophrenia, display NMDAR hypofunction, disrupted inhibitory transmission, hyperexcitability in the PFC, as well as deficits in working memory and learning (Carlson et al, 2011; Glen et al, 2014; Karlsgodt et al, 2011; Yuan et al, 2015). …”