In addition to the apparent changes in serotonergic and noradrenergic contributions to the effects of cocaine in DAT KO mice, there are other profound changes in these mice. As a consequence of the deletion of DAT in DAT KO mice, basal extracellular dopamine levels are extremely high in the dorsal striatum and nucleus accumbens (Rocha, et al., 1998; Shen, et al., 2004), apparently a result of dramatically reduced dopamine clearance (Mateo, Budygin, John, Banks, et al., 2004), while other aspects of dopamine function are substantially reduced, including levels of postsynaptic receptors, autoreceptor function and dopamine synthesis (Gainetdinov, Jones, & Caron, 1999; Giros, et al., 1996; Jones, et al., 1999; Sora, et al., 1998). However, one of the more interesting consequences of DAT deletion is that not all dopamine regions are affected in the same manner. Extracellular dopamine levels in the prefrontal cortex are unaffected in DAT KO mice (Shen, et al., 2004) or which is consistent with NET being the primary mediator of dopamine uptake in the prefrontal cortex (Mazei, Pluto, Kirkbride, & Pehek, 2002). One of the results of
