VTA DA neurons express a robust GABABR-activated GIRK current (IBaclofen) (Arora et al., 2011; Cruz et al., 2004; Padgett et al., 2012). In pre-conditional Snx27fl /fl littermates (referred to as wild-type; WT) and DAT-Cre+/− controls, bath application of a saturating concentration of the GABABR agonist baclofen (300µM) activated a large outward GABABR-activated GIRK current (203.6 ± 21.3 pA, n=17 for WT; 246.1 ± 24.6 pA, n=18 for Dat-Cre+/−); IBaclofen was completely suppressed by the selective Kir channel inhibitor Ba2+ (Cruz et al., 2004) (Figure 2A). In DA neurons of SNX27DA KO mice the GABABR-activated GIRK current was ~60% smaller; 74.7 ± 9.2 pA, n=18 (**p<0.01, one-way ANOVA with Bonferroni post hoc test) (Figure 2B). Dopamine D2R-activated GIRK currents revealed with bath application of quinpirole (30 µM) were similar in size for SNX27DA KO and control mice (Figure 2C,D), 47.0 ± 9.1 pA, n=13 for WT; 54.3 ± 14.2 pA, n= 8 for Dat-Cre+/− and 34.9 ± 9.1 pA, n= 14 for SNX27DA KO, p > 0.05). To investigate the potential effect of SNX27 KO on fast GABAA currents, we measured
