Figure 4. Averaged 24-activity profiles for all control and MPTP-treated monkeys with individual traces for all recordings (n = 39 assays) in LD (upper panel) and in LL (lower panel) conditions (A).

Data for LD always correspond to the recording period immediately preceding LL. Control (or pre-treatment) animals show a robust daily and circadian rhythmicity with a consolidated activity during the light phase in LD and the subjective day in LL. In MPTP-treated animals, the daily rhythmicity of locomotor activity in the LD cycle is clearly evident but becomes progressively less robust in non-symptomatic, mildly symptomatic and highly symptomatic animals. When transferred to constant LL conditions, circadian rhythmicity deteriorates and highly symptomatic animals are arrhythmic with a continuous distribution of activity throughout the 24 h period. Note that the loss of rhythmicity is also recorded in one asymptomatic animal under LL (also shown in Fig. 2B ). Relationship between the amplitude of the rhythm (χ² periodogram) and clinical score in LD and LL (B). A complete loss of rhythmicity is mainly, but not exclusively observed for the highest clinical scores whereas some subjects with severe motor symptoms still maintained rhythmicity. Values are shown as mean ± SEM. MPTP treatment induced loss of dopamine neurons in the mesencephalon and dopaminergic depletion of the striatum (C). Examples of [¹¹C]-PE2I scans of the basal ganglia before (C₁) and after MPTP treatment showing 69% decrease in [¹¹C]-PE2I binding potential in the striatum (C₂) and 86% in a more extreme case (C₃). The reduction of TH immunostaining in the mesencephalon of MPTP-treated monkeys (C₅, 65%, C₆, 72%, C₇, >80%) compared to a control (C₄). a: Substantia nigra (SN); b: Ventral tegmental area (VTA), Scale bar: 1000 µm.