cocaine exposure in the NAc and has been shown to be critically involved in behavioral responses to cocaine (Bowers et al., 2004). The stability and persistence of ΔFosB during weeks of drug withdrawal further support its role as a key regulator of AGS3 transcription during this period. Examples of genes where ΔFosB is associated with promoter hyperacetylation are Grin2a (NDMAR2A subunit) (Hemby et al., 2005), Per1 (Period 1), and Adora1 (Adenosine receptor A1) (Toda et al., 2002), each of which is known to be upregulated after chronic cocaine exposure and implicated in behavioral responses to cocaine (see Table 1). Together, these data indicate that the induction of ΔFosB in the NAc by cocaine regulates numerous gene targets, which now offer a much more complete understanding of the complex mechanisms by which this transcription factor mediates sensitized drug reward.
