Figure 3.

Mild dopaminergic deficits do not contribute to motor deficits in Tau^−/−-mice. (A–C) Levels of dopamine (A) and tyrosine hydroxylase (TH) in the striatum (B, C) were measured in mice of the indicated genotypes at 9–11 months (n=5 per genotype), 14–20 months (n=6–7 per genotype) or 25–26 months (n=7–10 per genotype) of age. RU, relative units; TH, tyrosine hydroxylase. (A) Striatal dopamine levels determined by HPLC. Two-way ANOVA: no effects of genotype (p=0.10) or age (p=0.14) and no interaction (p=0.40). (B) Representative western blot showing tyrosine hydroxylase (TH) levels in the striatum of two mice per genotype (age 25–26 months). Alpha tubulin served as a loading control. (C) Quantitation of striatal tyrosine hydroxylase by western blot analysis (n=4–10 mice per genotype and age as specified above). Two-way ANOVA: interaction (p=0.011), but no effects of genotype (p=0.72) or age (p=0.26). Average signals in two 25–26 month wildtype mice on each blot were arbitrarily defined as 1.0 and used to normalize signals across western blots. (D) Pole test deficits in middle-aged Tau knockout mice are not significantly improved by chronic treatment with L-DOPA/benserazide. Mice (n=11–14 per genotype, age: 12–15 months) were assessed in the pole test before and on the 7^th day of treatment with L-DOPA (200mg/L) and benserazide (50mg/L) in 0.2% ascorbic acid in their drinking water. Repeated measures two-way ANOVA: genotype effect (p=0.014) but no treatment effect (p=0.97) or interaction (p=0.71). *p<0.05 vs. age-matched wildtype mice (Bonferroni post hoc test of selected columns). Data are means ± SEM.