Likewise, results of the present study provide novel insight into the target genes through which ΔFosB and CREB contribute to the genomic effects of cocaine. Several genes previously identified as targets of ΔFosB and CREB, inferred from gene expression array studies of mice overexpressing the transcription factors or their dominant negative antagonists in the NAc (McClung and Nestler, 2003), were identified in this study. Examples include neurogranin, Period 1, GABAA receptor subunits, and MEF2C, to name a few. The present findings thereby indicate that many of the ΔFosB and CREB target genes determined through overexpression studies are indeed direct, physiological targets for these transcription factors in the NAc in vivo. Although to the best of our knowledge there have been no prior genome-wide ChIP-chip studies for FosB or ΔFosB, we should note that many of the phospho-CREB-bound genes observed here after chronic cocaine exposure (e.g., Pdyn, c-Fos, Mef2c, Cdk5) were also identified as CREB targets by previous CREB ChIP-chip studies (Impey et al., 2004; Tanis et al., 2007; Zhang et al., 2005). While it is known that CREB targets can
