Unilateral 6-OHDA lesions were performed on 190–305 g rats, as described previously (Magill et al., 2001 (link)). Twenty-five min before the injection of 6-OHDA, all animals received a bolus of desipramine (25 mg/kg, i.p.; Sigma) to minimize the uptake of 6-OHDA by noradrenergic neurons (Schwarting and Huston, 1996a (link)). Anesthesia was induced and maintained with isoflurane (as above). The neurotoxin 6-OHDA (hydrochloride salt; Sigma) was dissolved immediately before use in ice-cold 0.9% w/v NaCl solution containing 0.02% w/v ascorbate to a final concentration of 4 mg/ml. Then 3 μl of 6-OHDA solution was injected into the region adjacent to the medial substantia nigra (4.5 mm posterior and 1.2 mm lateral of bregma, and 7.9 mm ventral to the dura) (Paxinos and Watson, 1986 ). The extent of the dopamine neuron lesion was assessed 14 or 15 d after 6-OHDA injection by challenge with apomorphine (0.05 mg/kg, s.c.; Sigma) (Schwarting and Huston, 1996b (link)). The lesion was considered successful in those animals that made ≥80 net contraversive rotations in 20 min. Note that the emergence of exaggerated β oscillations after 6-OHDA lesions is not dependent on apomorphine (Sharott et al., 2005 (link)). Electrophysiological recordings were performed ipsilateral to 6-OHDA lesions in anesthetized rats 21–45 d after surgery, when pathophysiological changes in the basal ganglia are likely to have leveled out near their maxima (Vila et al., 2000 (link)).