FIGURE 3.

H₃R agonist-induced ERK 1/2 phosphorylation in striatal slices from wild-type and dopamine D₁R knock-out mice. Wild-type (white) or D₁R knock-out mice (black) slices were treated for 10 min with 0.1 μm RAMH or for 10 min with 10 μm thioperamide and/or 10 μm SCH 23390 prior to the addition of 0.1 μm RAMH and incubation for further 10 min. ERK 1/2 phosphorylation was determined as described under “Experimental Procedures.” For each treatment, the immunoreactive bands from four to six slices from a total six wild-type and nine knock-out animals were quantified, and values represent the mean ± S.E. of the percentage of phosphorylation relative to basal levels found in untreated slices (100%). No significant differences were obtained between the basal levels of the wild-type and the D₁R knock-out mice, and no significant differences were observed between basal and slices treated (20 min) with 10 μm thioperamide or 10 μm SCH 23390. Significant treatment and genotype effects were analyzed by a bifactorial analysis of variance followed by post hoc Bonferroni's tests. There were significant genotype, treatment, and interaction effects, explained by the ability of RAMH to strongly and selectively induce ERK 1/2 phosphorylation in wild-type mice (***, p < 0.001, as compared with knock-out mice). A representative Western blot is also displayed (top).