Ketamine

(±)-threo-ethylphenidate hydrochloride (EPH) was purchased from Cayman Chemical (Ann Arbor, MI, United States). Ketamine was purchased from Henry Schein Animal Health (Dublin, OH, United States) and xylazine and heparin (10 units/mL) from Sigma-Aldrich (St. Louis, MO, United States). Paraformaldehyde ampules were obtained from Electron Microscopy Sciences (Hatfield, PA, United States).

Stereotaxic surgeries were performed as described previously^{39 (link)}. Mice were anesthetized with a mixture of ketamine (100 mg/kg/10 ml) and xylazine (10 mg/kg/10 ml) (Henry Schein) in sterile saline. HSVs (-Gadd45b miR or -GFP) or BDNF (0.25 µg/side, recombinant human BDNF, R&D Systems) were bilaterally infused into the NAc (AP = 1.5, ML = ±1.5, and DV = −4.4 mm; 10° angle), while an AAV2 vector expressing ChR2, fused with enhanced yellow fluorescent protein (AAV2-EYFP-ChR2, purchased from University of North Carolina Vector Core) or its control (AAV2-EYFP), was infused into the VTA (AP = −3.2, ML = ±1.0, and DV = −4.6 mm; 7° angle). An infusion volume of 0.5 µl was delivered using 5 μL Hamilton syringe (Hamilton Company) over the course of 5 min (at a rate of 0.1 μl/min). Mice were allowed to recover for 4 days following the HSV infusion or for 7 days following the BDNF infusion before going through behavioral assessment. For the optogenetic stimulation of the VTA-NAc pathway, optic fibers were bilaterally implanted into the NAc (AP = 1.5; ML = ±1.3; DV = −3.9; 0° angle), three weeks after AAV2-EYFP-ChR2 or AAV2-EYFP infusion into VTA. Mice were allowed to recover for seven days following the cannulation, and then stimulated in home cages.