Fig. 2

Summary of schizophrenia-related phenotypes in various GluN1 mutant mice, in which GluN1 knockout is targeted to GABA neurons. GluN1 deletion during the embryonic stage in migrating forebrain Dlx5/6-positive GABAergic cells lead to lethality(Dlx5/6 cre KO). In contrast, GluN1 deletion after postnatal 4 weeks in PV neurons (PV-cre KO) or after adolescence in Ppp1r2-positive GABA neurons (bottom strain) produce less phenotypes compared to the mutant mice that received GluN1 deletion in GABA neurons in early postnatal period (Ppp1r2 cre-KO starting from PND 7). Thus, it appears that early postnatal period, but not during the embryonic stage or after adolescence, is a critical period of GABAergic NMDAR hypofunction leading to schizophrenia. arrow shows the period of knockout occurring in the designated KO cell-type in the cortex. The level of intrinsic property maturation of neocortical fast-spiking neurons largely based on Refs. 68,69. Relative change in synaptic evoked NMDA component estimated from the data in Ref. 22 for hippocampal PV neurons and Ref. 65 for mPFC PV neurons. Hyphen denotes no data. The data of Dlx5/6 cre-KO mice is unpublished. ROS reactive oxygen species. PPI, prepulse inhibition of startle reflex