limbic structures to synthesize the appropriate synaptic and behavioral responses to rewarding stimuli including drugs of abuse [1, 3]. Addictive drugs such as cocaine have been shown to induce long-lasting structural, electrophysiological, and transcriptional changes in the NAc, and some of these changes have been linked to addictive behaviors such as drug self-administration and relapse [1–4]. One of the best studied examples is the transcription factor ΔFosB, a splice product of the immediate early gene fosB, which accumulates several fold in the NAc after repeated drug exposure due to its protein stability [6–8]. The drug-induced accumulation of ΔFosB contributes to addiction-related behaviors, as its overexpression in the NAc sensitizes mice to the locomotor-activating and rewarding effects of cocaine and morphine [9, 10], as well as promotes the motivation to self-administer cocaine [11]. In addition to ΔFosB, gene expression microarrays have been used to identify other dysregulated genes in the NAc that may also contribute to the addicted state [12–18]. These genome-wide studies begin to illustrate the potent regulatory control drugs of abuse have on gene activity in the NAc, as numerous genes are up- or down-regulated in response to chronic drug exposure. While much is known about the upstream signaling
