Figure 4. Effects of 5-HT_1AR stimulation on D1R agonist-related striatal glutamate and AIMs in 6-OHDA- and sham-lesioned rats.

Rats in the second experiment received unilateral 6-OHDA or sham lesions of the MFB and 3 weeks later were primed with the D1R agonist SKF81297 (SKF; 0.8 mg/kg, sc) every 2–3 d for a total of 3 d. Dyskinetic (n=9) and sham-lesioned rats (n=7) underwent a microdialysis procedure including: 40 min baseline, 120 min vehicle treatment, 120 min drug treatment, and 60 min post-drug treatment sampling (dialysate collected every 20 min). Drug treatment included: Vehicle (VEH; 0.9% NaCl) or the full 5-HT_1AR agonist ±8-OH-DPAT (DPAT; 1.0 mg/kg, sc), immediately followed by SKF (0.8 mg/kg, sc). AIMs were observed during this time. Lines depict the means ± SEM of striatal glutamate (A) and AIMs (C) for VEH+SKF (n=9) and DPAT+SKF (n=9) in 6-OHDA-lesioned rats. Results for sham-lesioned rats receiving VEH+SKF (n=6) and DPAT+SKF (n=7) are expressed in (D) and (F). Bars depict the means ± SEM concentrations of striatal glutamate (M) during the 120 min of vehicle (VEH+VEH) and 120 min of drug treatments in 6-OHDA- (B) and sham-lesioned (E) rats. Effects over time were determined by two-way mixed design ANOVAs for striatal glutamate (% baseline). Striatal glutamate concentrations (M) were analyzed with oneway ANOVAs. Treatment effects for AIMs (expressed as medians) were analyzed by employing non-parametric Kruskal-Wallis tests. Significant differences between treatments were determined by Mann-Whitney post hoc comparisons for AIMs and planned comparison tests for striatal glutamate (% baseline and M).

* p < 0.05 for VEH+SKF vs DPAT+SKF