Fig. 6

GluN2B mutations and NMDAR-mediated evoked (e)EPSCs. a Pharmacological characterisation of NMDAR-mediated EPSCs from 13–15 DIV untransfected hippocampal neurons. Bar graphs report mean peak EPSC amplitude (left) and decay time (right) in the presence of either 3 μM ifenprodil (n = 15) or 30 μM TCN213 (n = 5), as a percentage of control EPSC values (dashed line, =100%). All bars are mean ± s.e.m. Two-tailed paired t-test *p < 0.05; **p < 0.005; ***p < 0.0005. b, c Bar graphs of peak amplitude (b) and weighted decay time constant (c) for evoked EPSCs for GluN1–GluN2B^WT and GluN2B mutant NMDARs. One-way ANOVA with Dunnett’s post-hoc test *p < 0.05. d–h Evoked and spontaneous EPSCs recorded at −70 mV from hippocampal neurons expressing GluN2B^WT (d), GluN2B^C461F (e), GluN2B^P553L (f), GluN2B^N615I (g) and GluN2B^V618G (h). In this and succeeding figures, red traces represent averaged EPSCs of 20 sweeps and the black dots indicate the presynaptic stimulation time point. Numbers of cells (n): GluN2B^WT n = 25, GluN2B^C461F 9, GluN2B^P553L 15, GluN2B^N615I 11, GluN2B^V618G 13. Calibration in d applies to other panels e–h