**2.2 6-OHDA lesion**

Unilateral 6-OHDA lesions were made in the mice and rats when they were 8-weeks old. We aimed for partial (40-60%) loss of SNc DA neurons because another form of compensatory plasticity (i.e. spouting of surviving nigrostriatal projections) in the nigrostriatal system is hampered with lesions >75% (Stanic et al. 2003). Mice were anesthetized with an i.p. injection of 5% chloral-hydrate in sterile phosphate buffered saline, whereas rats were anesthetized with 1-2% isofluorane in air. Their heads were secured in a stereotaxic frame and a midline incision made over the skull. A small (2-3mm diameter) hole was drilled through the skull overlying the left (mice) or right (rats) SNc with a dental burr. In mice, 1.5µg/µl 6-OHDA (Sigma-Aldrich) in distilled H2O with 0.2mg/ml ascorbic acid was prepared on the morning of the lesions and kept on ice until injected to minimize oxidation. 1.6µl of the 6-OHDA solution was injected slowly (1.0µl/min.) through a 26gauge sterile needle at stereotaxic coordinates: 3.0mm posterior to Bregma, 1.5mm lateral to the midline, 4.0mm deep. In rats, two 1.0µl injections of 2.0µg/µl 6-OHDA in distilled H2O with 0.2mg/ml ascorbic acid were made through a glass micropipette at stereotaxic coordinates: (1) 3.7mm anterior to Lambda, 1.7mm lateral to the midline, 8.1mm deep; and (2) 3.7mm anterior to Lambda, 2.1mm lateral to the midline, 7.5mm deep. At the completion of each injection the injection needle was left in situ for 2mins. to allow toxin diffusion then the needle was slowly withdrawn to minimize toxin backtracking up the needle track. The skin was sutured and antiseptic applied, an anti-inflammatory [3mg/kg Meloxicam (Metacam®), s.c.] was administered, and the animal was left to recover in a warmed cage.
