Expression of SNX27 is known to be important for mouse development (Cai et al., 2011). We therefore wanted to rule out the possibility that loss of SNX27 in DA neurons during neurodevelopment did not indirectly affect the expression of GIRK channels. To address this possibility, we expressed SNX27 selectively in DA neurons of 4-week-old SNX27DA KO mice and then measured the amplitude of GABABR-activated GIRK currents in DA neurons after 2–3 weeks. Both splice variants, SNX27a and SNX27b, are developmentally regulated (Kajii et al., 2003). Because SNX27b is sensitive to psychostimulants (Kajii et al., 2003), we engineered Snx27b into an adeno-associated virus (AAV; serotype 5), with a double floxed inverted (DIO) Snx27b-ires-GFP sequence under the control of EF1a promoter (Tsai et al., 2009) (Figure 5A). In the DAT-Cre+/− line, injection of AAV DIO Snx27b-ires-GFP limits expression of SNX27b to neurons containing Cre recombinase, which is expressed in DAT+ neurons. For control, we studied the effect of injecting AAV DIO-eYFP, a similar virus that lacks SNX27b. In SNX27DA KO mice with either AAV DIO Snx27b-ires-GFP or AAV DIO-eYFP stereotaxically injected into
