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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Behav Brain Res. 2018 Jun 25;353:124–128. doi: 10.1016/j.bbr.2018.06.029

Fig. 1. Absence of CIE-potentiation of EtOH drinking in GluN2A knockout mice.

Fig. 1.

(A) Schematic of the timeline for pre-CIE EtOH drinking, CIE (or air) exposure and post-CIE drinking in GluN2A knockout (KO) mice and their wild-type (WT) litter mate controls. (B) CIE-induced blood EtOH concentration (BECs) did not differ between genotypes. (C) Body weight did not differ between genotypes, irrespective of CIE-exposure. (D) Pre-CIE EtOH consumption did not differ between genotypes. Post-CIE EtOH consumption was significantly higher in CIE-exposed WT mice, as compared to either air-exposed WT mice or CIE-exposed KO mice. (E) Pre-CIE EtOH preference did not differ between genotypes. Post-CIE EtOH preference was significantly higher in CIE-exposed WT mice relative to CIE-exposed KO mice. Data are mean ± SEM. n =6–12 per genotype per treatment group. *P < .05 WT AIR versus WT CIE or WT CIE versus KO CIE.