Figure 4.

ΔFosB is both necessary and sufficient for cocaine-mediated D₁ receptor-dependent CaMKIIα induction in NAc shell. A, AAV-mediated overexpression of ΔFosB in NAc shell promotes locomotor responses to an acute cocaine injection in adult male rats. B, Western blot analysis of NAc shell shows that ΔFosB is sufficient to increase levels of total CaMKIIα and both autophosphorylation of CaMKIIα and Ser831 phosphorylation of GluA1; quantified in C (n = 14–18; *p < 0.05, two-tailed t test). D, AAV-mediated ΔJunD overexpression prevents locomotor sensitization induced by chronic exposure to cocaine. E, ΔJunD overexpression in NAc shell is sufficient to block cocaine-mediated increases in total and Thr286 phospho-CaMKII and to reduce levels of ΔFosB in both saline- and cocaine-treated animals; quantified in F (n = 8–10; *p < 0.05, one-way ANOVA).