Figure 6.

Blockade of CaMKII activity prevents the morphological and behavioral effects of ΔFosB in NAc. A, Increases in the spine density of MSNs in NAc shell induced by HSV-mediated overexpression of ΔFosB are prevented by coexpression of the CaMKII inhibitor peptide AC3I (n = 14–16); quantified in B. C–E, ΔFosB effects on thin and stubby spines are blocked by coexpression of AC3I. F, The ΔFosB-mediated increase in locomotor sensitivity to cocaine is also prevented by AC3I coexpression. G, Model depicting the D₁-receptor-dependent induction of a CaMKII/ΔFosB feedforward loop by cocaine, including upstream signaling cascades and physiological processes that may be affected. DA, Dopamine; D1DR, D₁ dopamine receptor; LTCC, L-type calcium channel (n = 9–10; *p < 0.05, one-tailed t test).