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. 2016 Oct;109:69–77. doi: 10.1016/j.neuropharm.2016.05.013

Fig. 1.

Fig. 1

α-Synuclein-induced motor deficits and dopaminergic neurodegeneration. A. Stepping test performances at Baseline (0), 4, 8 and 12 weeks after viral-mediated expression of α-synuclein in the substantia nigra (p < 0.001 for each time-point; 2-way RM-ANOVA); B. Motor performances at 12 weeks post-surgery for the 3 subgroups of each population (*p < 0.001 from sham; 2-way ANOVA); C. Stereological counts of tyrosine hydroxylase (TH) positive cells in the Substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA), *p < 0.0001 (t-test; all impulsivity traits included); D. Magnitude of the nigral lesion in Low impulsive (LI), Intermediate (Int) and High impulsive (HI) animals (*p < 0.05 from Lesioned LI and Int; 2-way ANOVA); F. Representative mesencephalic sections of one sham rat and lesioned rats of each impulsivity subgroup (upper panel) stained for TH. Low magnification pictures of α-synuclein immunostaining in each subgroup (middle panel; scale bar: 100 μm). High magnification images of the corresponding LI, Int and HI animals (lower panel; scale bar: 20 μm) showing α-synuclein accumulation in all subgroups. Sh = sham; LI = low impulsive; Int = intermediate; HI = high impulsive. Data represent mean ± SEM. Sham: LI: n = 5, Int: n = 12, HI: n = 4; Lesioned: LI: n = 6, Int: n = 11, HI: n = 6.