Knowledge of early gene expression changes in response to drug exposure has largely derived from animal studies, many of which have focused on preselected candidate genes and pathways. The molecular targets are often drug specific, for example, the dopamine transporter for cocaine and amphetamine exposure (Calipari, Ferris, Salahpour, Caron, & Jones, 2013; Peraile et al., 2010), opioid receptors and propeptide genes for opioid exposure (Diaz, Barros, Antonelli, Rubio, & Balerio, 2006), and GABA and glutamate receptors for other drug and alcohol exposure (Enoch et al., 2012; Meinhardt et al., 2013; Nona, Li, & Nobrega, 2013; Schumann & Yaka, 2009; Swanson, Baker, Carson, Worley, & Kalivas, 2001; Zhang et al., 2009; Zhou et al., 2013). Certain aspects of cell signaling, early transcriptional response, and learning have been obvious, and fruitful, targets for study in the addictions. Acute exposure to cocaine induces expression of immediate-early genes such as Jun and Fos, which encode transcription factors. The transcripts of these gene return to control levels, and following repeated administration of the drugs, desentization is seen (Hope, Kosofsky, Hyman, & Nestler, 1992). The transcription
