Figure 5
From: LSD-stimulated behaviors in mice require β-arrestin 2 but not β-arrestin 1
Effects of LSD, MDL100907, and haloperidol on prepulse inhibition in β-arrestin 1 mice. Mice were injected with MDL100907, haloperidol, or the vehicle and administered subsequently the vehicle or LSD prior to testing PPI. (a) PPI in WT and βArr1-KO mice treated with MDL or LSD. A RMANOVA found the main effects of prepulse intensity [F(1,91) = 487.507, p < 0.001], genotype [F(1,91) = 25.358, p < 0.001], and treatment [F(4,91) = 11.435, p < 0.001] to be significant. The prepulse intensity by genotype [F(1,91) = 9.162, p = 0.003], prepulse intensity by treatment [F(4,91) = 7.944, p < 0.001], genotype by treatment [F(4,91) = 2.394, p = 0.052], and prepulse intensity by genotype by treatment interactions [F(4,91) = 2.611, p = 0.041] were significant. (b) PPI in WT and βArr1-KO mice that received haloperidol or LSD. A RMANOVA detected significant main effects for prepulse intensity [F(1,72) = 415.876, p < 0.001], genotype [F(1,72) = 7.563, p = 0.008], and treatment [F(3,72) = 9.591, p < 0.001]. The prepulse intensity by treatment interaction was also significant [F(3,72) = 7.702, p < 0.001]. N = 8–12 mice/group. *p < 0.05, ***p ≤ 0.001, WT vs. KO; ++p < 0.01, LSD vs. indicated groups within genotype; ††p < 0.01, 0.1MDL + LSD vs. indicated groups within genotype.
