For example, neonatal repeated exposure to PCP,71 ketamine,57 or MK-80170 consistently disturbs the developmental GluN2B-GluN2A switch that occurs in immature PV neurons during PND 14–21.22 Consistently, a transcription factor called REST, which facilitates GluN2B-GluN2A switch in neurons, appears to be less functional in schizophrenia.148 If the increase of GluN2B subunit mRNA was detected in PV neurons of schizophrenia postmortem brains, in particular, at the earlier life stage, it might suggest NMDAR hypofunction in PV neurons in perinatal period. This evidence concerns the gene GRIN2B and schizophrenia.