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. Author manuscript; available in PMC: 2017 Apr 13.
Published in final edited form as: Cell Rep. 2017 Mar 21;18(12):2807–2814. doi: 10.1016/j.celrep.2017.02.075

Figure 4. Genetic reduction of β-arrestin2 does not potentiate the psychotomimetic effects of MK801.

Figure 4

WT and Arrb2+/− mice injected intraperitoneally with the NMDAR antagonist MK801 (0.3 mg/kg) show comparable hyperlocomotion 60 minutes post-treatment compared to vehicle (N = 10 mice per group). Data points represent distance travelled in cm over 5 minute bins, averaged as pooled animals per treatment group. Pre-treatment with MTEP (10 mg/kg, i.p.) potentiates hyperlocomotion in both WT and Arrb2+/− mice (N = 9 mice per group). Two-way ANOVA for genotype: F = 0.468, p = 0.499, and for treatment: F = 13.597, *p < 0.001; no significant interaction between genotype and treatment: F = 0.352, p = 0.557. Two-tailed t test, WT + MK801 vs. WT + MTEP + MK801: t = 2.9358, *p = 0.0092. Two-tailed t test, Arrb2+/− + MK801 vs. Arrb2+/− + MTEP + MK801: t = 2.2603, *p = 0.0372.