According to the most recent US statistics, ~15% of individuals aged 12 and older report having used cocaine at least once in their lifetime (National Survey on Drug Use and Health, 2015), and cocaine continues to be the most frequently cited drug of abuse during drug-related emergency room visits (Drug Abuse Warning Network, 2014). Relapse, frequently precipitated by exposure to drug-associated environmental cues (Rohsenow et al, 1990), is the most significant impediment in the treatment of cocaine addiction, and pharmacological interventions that disrupt the acute motivational effects of cocaine-paired cues or facilitate the establishment of inhibitory cue-no drug associations have been largely unsuccessful due to unfavorable off-target effects and temporary/context-dependent therapeutic effects, respectively (for review, see Torregrossa and Taylor, 2016). Thus, FDA-approved medications for cocaine addiction remain unavailable. However, reports of novel therapeutic targets, compounds, and methodological advances suggest that progress is being made toward the development of effective therapies for cocaine addiction. One such report is offered by Monsey et al (2016) in the current issue of Neuropsychopharmacology.

On the basis of research conducted in rats, the authors propose a novel experimental treatment that impairs cocaine-cue memories and subsequent cue-induced goal-directed behavior. The idea that the long-term memories of maladaptive associations can be weakened is a corollary of the memory reconsolidation hypothesis proposed by Nader et al (2000). They postulated that fear memories destabilize upon retrieval and must undergo a protein synthesis-dependent reconsolidation process in order to be maintained over time. Furthermore, according to more recent literature, drug memories undergo a similar reconsolidation process, and reconsolidation inhibitor manipulations applied following drug memory destabilization disrupt subsequent Pavlovian cocaine-conditioned responses and instrumental goal-directed behaviors in animal models of drug relapse (for review, see Hernandez and Kelley, 2005; Sorg, 2012; García-Pardo et al, 2016).

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