to as SNX27DA KO mice (Figure 1A–C). Importantly, SNX27DA KO mice were viable, bred normally and lived into adulthood. Moreover, the number of TH positive neurons in the VTA/SN did not appear to differ from control mice (Figure 1D). We next examined the viability of VTA DA neurons using whole-cell patch clamp electrophysiology in 3–4 week old mice. Dopamine neurons were identified by presence of an Ih current, slow firing frequency and by Cre-dependent expression of fluorescent proteins when available (Cruz et al., 2004; Labouèbe et al., 2007; Padgett et al., 2012). Other types of VTA DA neurons exist, which lack Ih and project to mPFC, but these neurons do not possess D2R-activated GIRK currents (Lammel et al., 2008). VTA DA neurons in acutely prepared horizontal midbrain slices from SNX27DA KO mice had input resistances, resting membrane potentials and cell sizes indistinguishable from those in wild-type neurons (Figure 1E & Supplemental Table 1). Similarly, loss of SNX27 in DA neurons did not significantly change the amplitude of Ih current (Figure 1F). Taken together, these results suggest that there were no gross changes in function of DA neurons lacking SNX27.
