Fig. 7

NMDAR-mediated synaptic transmission is altered at hippocampal Sch–CA1 synapses in KDM6B mKO mice. (A) Representative traces (left) and summary data (right) showing that the NMDAR/AMPAR ratio is lower in KDM6B mKO compared to control (Control, 1.12 ± 0.10; KDM6B mKO, 0.53 ± 0.09, p = 0.02). (B) NMDAR-EPSCs input output curve is decrease in KDM6B mKO compared to control. (C) Normalized NMDAR-EPSCs (left) and summary data (right) showing slower NMDAR decay kinetics in KDM6B mKO compared with control (Control, 50.30 ± 11.30; KDM6B mKO, 71.70 ± 18.36, p = 0.04). (D–E) Digital PCR assay to determine NR2A (D) or NR2B (E) cDNA copies/µl in WT and KDM6B mKO animals (WT n = 3; KDM6B mKO n = 4). (F) Averaged NMDAR-EPSCs (left) and summary data (right) showing more sensitivity to the selective NR2B antagonist Ro25-6981 (500 nM) in KDM6B mKO animals compared to control (Control, 71.24 ± 4.67; KDM6B mKO, 44.69 ± 4.65, p = 0.002) (G) Representative traces (left) and summary data (right) showing that NMDA-dependent LTP induced by high frequency stimulation (arrows) is impaired in KDM6B mKO compared with control animal. Averaged sample traces were taken at times indicated by numbers in the summary plot. In all panels, summary data represent the mean ± SEM and the number of cells (c), and animals (a) are indicated in parentheses. Student t-test was used for statistical analysis, *p < 0.05, **p < 0.01, ***p < 0.001.