termed 11A and 11B, which direct transgene expression to either D1+ or D2+ MSNs, respectively (Chen et al., 1998; Kelz et al., 1999; Werme et al., 2002). Line 11A mice crossed with a Tet-Op ΔFosB line show increased responses to the rewarding and locomotor effects of cocaine (Kelz et al., 1999), which is consistent with ΔFosB induction in D1+ MSNs (Nye et al., 1995; Moratalla et al., 1996). Furthermore, these same mice display increased morphine reward (evaluated by CPP) as well as diminished morphine analgesia and enhanced morphine tolerance, while the 11B Tet-Op ΔFosB mice show no change in morphine reward. Overexpression of a dominant negative antagonist of ΔFosB exerts effects opposite to those seen with ΔFosB, although this mouse model does not distinguish D1 vs. D2 MSNs (Peakman et al., 2003). Together, these data further supports the role of ΔFosB induction in D1+ MSNs as an important molecular player in the rewarding properties of drugs of abuse (Zachariou et al., 2006). This phenomenon is also observed in other reward behaviors, in particular, wheel running: 11A Tet-Op ΔFosB mice display increased wheel running behavior, whereas 11B Tet-Op ΔFosB mice display diminished wheel running (Werme et al., 2002). The finding that
