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Figure S1. Injection of 6-OHDA into the mfb resulted in nigrostriatal DA degeneration and expression of OX6+ve cells. 20 μm coronal sections taken at day 9 after 6-OHDA lesion induction were immunostained for TH or OX6 [recognises major histocompatibility complex (MHC) class II antigens]. Panel (a) (left) shows selective loss of TH immunoreactivity ipsilateral to the side of 6-OHDA injection. Neurons in the lateral portion (arrows) and ventral tier (arrowheads) of SNc were most vulnerable. Inserted box illustrates typical cytoplasmic staining in DA neurons (400×). Panel (b) (right) shows specific accumulation of OX6+ve cells at the site of neurodegeneration. Inserted box illustrates typical ramified morphology OX6+ve cells (400×).

Figure S2. Time-dependent unilateral depletion of striatal dopamine content following 6-OHDA lesion induction. Male Sprague–Dawley rats were injected with 12 μg 6-OHDA into the mfb (day 0) and killed at the indicated time points. Striata were removed and processed for HPLC-ECD to measure the striatal dopamine content. Results are expressed as mean (ng/mg) ±SEM. Dopamine deletion manifests from day 9 after 6-OHDA lesion induction and progresses to day 15 after lesioning. **p < 0.01, ***p < 0.001 compared to the non-lesioned side. n = 6 animals/per time point.

Table S1. Confidence intervals for the time dependent changes in the number of OX-42+ve, OX-6+ve and CD68+ve cells in the 6-OHDA lesioned and unlesioned side of the brain.

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