ΔFosB has been shown to play an important role in addiction: its overexpression in the NAc increases an animal’s responses to the rewarding effects of cocaine and of morphine, while overexpression of a dominant negative antagonist, termed ΔcJun, causes the opposite effects (Nestler, 2008). A previous gene expression array study identified genes in the NAc whose expression is altered upon overexpression of ΔFosB or ΔcJun (McClung and Nestler, 2003). However, this study could not provide information as to which of these genes are direct targets for ΔFosB or regulated indirectly via other mechanisms. To address this question, we carried out ChIP for ΔFosB in mice treated with chronic cocaine or saline. Since a change in the absolute level of a transcription factor on a given promoter is not necessarily an indication of its activity, we simply identified the gene promoters significantly occupied by ΔFosB under saline and cocaine-treated conditions independently. After pre-processing and normalization, we generated a high-confidence gene list at a false discovery rate of 5% using established methodology (see Supplemental Methods). In chronic cocaine-treated mice, ΔFosB was bound
