Figure 6. Chronic or acute l-DOPA induces phosphorylation of ERK and histone H3 in the lesioned striatum of Gnal heterozygous mice. A, B, Confocal sections through the dorsolateral striatum of unlesioned (UL) and 6-OHDA-lesioned dorsolateral striatum of Gnal+/+ (top row) and Gnal+/− (bottom row) mice, 30 min after the last injection of chronic l-DOPA and benserazide treatment showing phospho-ERK (pERK, A) and phospho-acetyl-histone H3 (pAcH3, B) immunofluorescence. Scale bar, 100 μm. Bottom graphs, Number of pERK- or pAcH3-positive cells in the dorsolateral striatum. Data are means ± SEM in 375 × 375 μm confocal images (n = 8–11). Repeated-measures two-way ANOVA (with the within-subjects factor of lesion and the between-subjects factor of genotype): A, pERK, effect of the lesion, F(1,17) = 67, p < 0.0001; effect of the genotype, F(1,17) = 0.89, not significant; interaction, F(1,17) = 1.03, not significant; B, pAcH3, effect of lesion, F(1,17) = 57, p < 0.0001; effect of genotype, F(1,17) = 0.02, not significant; interaction, F(1,17) = 0.01, not significant. Post hoc comparison (Bonferroni's test): ***p < 0.001, 6-OHDA versus unlesioned. C, D, Same as in A and B but in different groups of mice that received a single injection of l-DOPA (n = 4–8 per group). C, pERK, effect of lesion, F(1,20) = 893, p < 0.0001; effect of genotype, F(1,20) = 0.79, not significant; interaction, F(1,20) = 0.79; not significant. D, pAcH3, effect of lesion, F(1,20) = 1231, p < 0.0001; effect of genotype, F(1,20) = 3.61, not significant; interaction, F(1,20) = 3.61, not significant. Post hoc comparison (Bonferroni's test): ***p < 0.001, 6-OHDA versus unlesioned.