Over 34 million Americans aged 12 or over report lifetime use of cocaine, with an estimated 1 million new users of cocaine each year.1 The negative health and economic consequences of cocaine use on society are considerable, with cocaine use associated with potentially fatal cardiovascular events such as arrhythmias, myocardial infarction, and cerebral hemorrhage. In common with other substance-use disorders, cocaine addiction is characterized by a compulsive need to seek and take the drug, a loss of control over the amount of drug consumed, and by periods of attempted abstinence closely followed by relapse to drug-taking behavior.2 The mechanisms by which cocaine comes to dominate the behavioral repertoire in this manner remain unclear. Emerging evidence suggests that cocaine and other addictive drugs modify the transcriptional landscape of neurons in brain reinforcement circuits and drive the increasing control over behavior exerted by the drug. Cocaine can modify gene expression, and hence neuronal function, at the transcriptional and translational level. Much current work is focused on understanding the chromatin-modifying actions of cocaine that influence gene expression levels.3 However, far less is known
