Furthermore, when the NR1 subunit was selectively eliminated in parvalbumin-positive interneurons in forebrain cortices and hippocampus in early (neonatal) development, the rats exhibited reduced glutamic acid decarboxylase 67 (GAD67) and parvalbumin as well as distinct schizophrenia-related symptoms that emerged after adolescence; in contrast, post-adolescent deletion of NR1 did not result in such abnormalities (Belforte et al., 2010). The gene discussed is PVALB; the disease is schizophrenia.