Skip to main content
. 2017 Nov;363(2):148–155. doi: 10.1124/jpet.117.242321

Fig. 3.

Fig. 3.

Ethanol (EtOH) upregulation of NMDAR-mediated transmission is absent in AC1KO (KO) mice. (A) Representative traces of NMDAR-mediated eEPSCs and (B) average NMDAR-mediated eEPSC amplitude (± S.E.M.) in WT and AC1KO mice repeatedly treated with saline (sal) or EtOH. EtOH produced an increase in NMDAR-mediated eEPSC amplitude only in WT mice (two-way ANOVA and Sidak’s post hoc test, **P < 0.01). (C) Average NMDAR-mediated eEPSC amplitude before (BL) and after (+Ro) bath application of the GluN2B selective antagonist Ro 25-6981 (0.5 µM) in WT mice. EtOH-induced upregulation of NMDAR-mediated transmission involved an increased contribution of GluN2B-containing NMDARs (two-way RM ANOVA and Sidak’s post hoc test, *P < 0.05). (D) Average central location of medium spiny neuron recordings was 1.10 mm from bregma (± 0.5 mm).