6ohda

Mice were anesthetized with 2% isoflurane and secured on a stereotactic frame. 6-Hydroxydopamine (6OHDA; 2547; Tocris) was dissolved in a 0.2% ascorbic acid saline solution. A 0.2% ascorbic acid saline solution was used as vehicle control. WT mice received a unilateral injection of 6OHDA or vehicle control in the striatum. The striatum coordinate used for stereotaxic injection was AP = 0.7 ML = − 2.0 DV = − 2.0 mm. A total of 5 μg of 6OHDA in 2 μL was injected in the striatum at a rate of 0.5 μL/min with a 33G nanofil blunt needle (NF33BL-2, World Precision Instruments) connected to FEP tubbing and a 25 μL Hamilton syringe. After 6OHDA infusion, the nanofil blunt needle was left in place for 5 min. Four weeks after injection, mice were PBS and 4% PFA perfused for immunohistochemistry analysis.

The dopaminergic innervation of the left dorsal striatum of Lhx6-iCre;RCE-EGFP mice (25–40 g, aged postnatal day 30 (P30) to P40) was destroyed by local stereotaxic injection of 6-OHDA (Sigma-Aldrich, Inc., USA) under 5% ketamine (Imalgène^® 1000, Merial SAS, France)/2.5% xylazine (Rompun^® 2%, Bayer SAS, France) anesthesia (10 μl g⁻¹, intraperitoneally (i.p.)). Two microinjections of 6-OHDA were performed through a NanoFIL syringe (outside diameter, 135 μm; World Precision Instruments, USA) placed into the left dorsal. For sham-operated animals, we injected an equivalent volume of vehicle (sterile saline 0.9%), ascorbic acid 0.05%, pH 7.4. We performed in vitro recordings 15–20 days after lesion. The efficacy of the 6-OHDA-induced lesion of dopaminergic terminals in the striatum was determined 10 days before the recording session by apomorphine-induced rotation (0.5 mg kg⁻¹ in 0.1% ascorbic acid, i.p.)^{44 (link)}. We checked the extent of the lesion after the recording session by immunohistochemical visualization of tyrosine hydroxylase (TH) in the striatum (see Supplementary Fig. 11).