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 ΔFosB induction in D1 MSNs promotes reward is consistent with recent findings that such cell-type-selective induction also promotes resilience responses to chronic stress (Vialou et al., 2010). Finally, chronic cocaine induction of ΔFosB in D1+ MSNs was shown to be accompanied by robust long-lasting increases in dendritic spine densities (Lee et al., 2006) and recently ΔFosB in the NAc was shown to be both necessary and sufficient in mediating the increased density of dendritic spines in this brain region (Maze et al., 2010). Such data support a role for ΔFosB in D1+ MSNs in mediating the rewarding aspects of drugs of abuse and natural rewards as well as the accompanying structural plasticity changes. The data also suggest that induction of ΔFosB in D2+ MSNs confers negative consequences to rewarding stimuli. Since ΔFosB induction in D2+ MSNs is seen in response to chronic stress and antipsychotic drug exposure (Hiroi and Graybiel, 1996; Perrotti et al., 2004), further studies of the latter
