Parkinson’s disease (PD) is characterized by reduced dopamine levels in the striatum causing severe motor deficits. Patients are thus often treated with L-DOPA, the precursor of catecholamines, including dopamine, but positive effects of this treatment fade with prolonged treatment resulting in dyskinesia. To model this priming effect of L-DOPA treatment in vivo, Wistar Han rats can be utilized. Animals are unilaterally lesioned by injecting 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle to induce typical PD symptoms.
For L-DOPA priming, rats are treated intraperitoneally with L-DOPA for 21 days starting 3 weeks after lesioning.
For the evaluation of L-DOPA-induced dyskinesia (LID) rats are treated once with vehicle, 3 mg/kg, or 6 mg/kg L-DOPA about 2 weeks after the priming phase and afterwards analyzed in the ALO test to evaluate axial, limb and orolingual abnormal involuntary movements. Furthermore, rats are tested in the Rotometer bowl to evaluate contralateral rotations. The results show that L-DOPA induces a strong increase in the ALO score (A), and contralateral rotations (B) compared to vehicle-treated rats. Additionally, this effect was strongly dependent on the concentration of L-DOPA.
Figure: ALO and rotation test after ICV 6-OHDA injection and L-DOPA priming. The ALO score (A) and the percentage of contralateral rotations (B) after acute L-DOPA treatment. n = 6 per group; mean + SEM; two-way ANOVA followed by Tukey’s multiple comparison post hoc test (A) and one way ANOVA followed by Tukey’s multiple comparison post hoc test; *p<0.05, ***p<0.001.
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