Fig. 2

The GluN2C/2D components of the NMDAR-mediated EPSCs are significant in neurons of the ACC by using UBP145 as the antagonist of GluN2C/2D. a A selective GluN2C/2D antagonist, UBP145, partially inhibited NMDAR-mediated EPSCs. Left: the time course of changes in EPSC amplitude before, during and after the application of UBP145 (3 μM) in ACC neurons from adult male mice is shown. Traces show the currents at different time points during application of drugs. UBP145 produced its maximal effect at 20 min after bath application and was partially washed out (n = 5 neurons/3 mice). Right: Summary of the partial inhibition of the UBP145 on the NMDAR-mediated current. Data within the last five minutes of the baseline, UBP145 application and washout phase is averaged. Open circles represent the individual data points. b Summarized data of the effect of UBP145 to the rising time (left) and decay time (right) of the NMDAR-mediated EPSCs in the ACC neurons. The application of UBP145 produced a significant inhibitory effect on the decay time of EPSCs. c Left: application of the antagonist of the GluN2A (PEAQX) and GluN2B (Ro 25-6981) reduced over 60% of the NMDAR current. UBP145 further decreased the amplitude of EPSC. The remaining current were gradually decreased by the application of AP-5. Right: Summary of the gradual inhibition of the GluN2A/2B and GluN2C/2D on the NMDAR-mediated current. * p < 0.05, *** p < 0.001, compared with baseline; # p < 0.05, compared with PEAQX + Ro25-6981. Error bars represent SEM