Figure 3.

The development of dyskinesia and the associated angiogenic activity are dose-dependently induced by chronic l-dopa treatment. (A) Development of dyskinesia during 21 days of treatment, high-dose l-dopa (25 mg/kg, n = 6), low-dose l-dopa (6 mg/kg, n = 6), saline-treated controls (n = 6). Abnormal involuntary movement scores are expressed as the sum of limb, axial and orolingual scores per session. Repeated measures ANOVA followed by Tukey’s Honestly Significant Difference post hoc comparison. (B–E) Indices of angiogenesis and increased blood–brain barrier permeability in the striatum and substantia nigra pars reticulata (SNr) are dose-dependently regulated by l-dopa treatment. (Left) Data from the striatum; (right) data from the substantia nigra pars reticulata, from the same animals as in (A). (B) Endothelial proliferation (counts of bromodeoxyuridine-labelled cells on laminin-positive blood vessel profiles); (C) upregulation of nestin on blood vessel profiles; (D) Downregulation of endothelial barrier antigen (EBA) in blood vessels, and (E) parenchymal albumin extravasation. One-factor ANOVA followed by post hoc Student–Newman–Keul’s, P < 0.05; *versus saline, ^#versus l-dopa low-dose group. All values are expressed as mean ± SEM.