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Opening the genome to reduce cocaine-seeking behavior

Since the discovery of specific mechanisms regulating gene transcription, studies have explored therapeutic avenues in the treatment of disease through such epigenetic targets, including the mechanisms of histone acetylation/deacetylation. Indeed, compounds that inhibit histone deacetylation [i.e., histone deacetylase (HDAC) inhibitors] have been investigated as treatments for a variety of diseases, including cancer (1), Alzheimer’s disease, and Parkinson disease (2). Considering the role that transcription plays in learning and memory (3), it is not surprising that memory-related diseases and disorders are particularly ripe for treatments based on epigenetic targets. In PNAS, Malvaez et al. (4) report that systemic administration of a selective HDAC3 inhibitor to rats enhances the extinction of cocaine-seeking, consistent with previous work (5, 6). Crucially, they demonstrate that the enhanced extinction is rapid and persistent and even appears to eliminate the reinstatement of cocaine-seeking, suggesting the potential for targeting this mechanism as an adjunctive therapy. Moreover, the authors use a unique behavioral design that enables them to distinguish the effects of the HDAC inhibitor on extinction consolidation from effects on reconsolidation and performance.