4.3. Unilateral 6-OHDA Lesion

We performed standard unilateral 6-OHDA denervation in the left hemisphere [6,27] to obtain chronic DA-depleted animals. The animals (399 ± 36.3 g) were anesthetized with 1.5%–2.5% isoflurane in oxygen and then injected with desipramine (25 mg/kg, i.p.) and pargyline (50 mg/kg, i.p.) to minimize 6-OHDA uptake by noradrenergic neurons and metabolism by MAO, respectively. Then, the animals were mounted on a stereotaxic instrument (Stoelting Co., Wheat Lane, Wood Dale, IL, USA) for injection of the neurotoxin (6-OHDA; Sigma; 8 µg/4 µL of saline solution containing 0.1% of ascorbic acid) in the medial forebrain bundle (MFB; stereotaxic coordinates: 2.5 mm posterior to the bregma, 2 mm lateral to the midline, and 8.6 mm below the cortical surface) [44]. The MTh neuronal activity was recorded an analyzed in 6-OHDA-lesioned rats (n = 8) and control animals (n = 6). The microdialysis experiments were performed in sham animals (n = 9), receiving instead, 4 µL of saline solution containing 0.1% of ascorbic acid infused into the MFB and 6-OHDA-lesioned animals (n = 9). Electrophysiological and microdialysis experiments were performed 21–29 days after the administration of 6-OHDA