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Neuropsychopharmacology. 2013 Jan;38(1):94-110. doi: 10.1038/npp.2012.154. Epub 2012 Aug 22.

The role of histone acetylation in cocaine-induced neural plasticity and behavior.

Author information

1
Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory, University of California, Irvine, 301 Qureshey Research Lab, Irvine, CA 92697-3800, USA.

Abstract

How do drugs of abuse, such as cocaine, cause stable changes in neural plasticity that in turn drive long-term changes in behavior? What kind of mechanism can underlie such stable changes in neural plasticity? One prime candidate mechanism is epigenetic mechanisms of chromatin regulation. Chromatin regulation has been shown to generate short-term and long-term molecular memory within an individual cell. They have also been shown to underlie cell fate decisions (or cellular memory). Now, there is accumulating evidence that in the CNS, these same mechanisms may be pivotal for drug-induced changes in gene expression and ultimately long-term behavioral changes. As these mechanisms are also being found to be fundamental for learning and memory, an exciting new possibility is the extinction of drug-seeking behavior by manipulation of epigenetic mechanisms. In this review, we critically discuss the evidence demonstrating a key role for chromatin regulation via histone acetylation in cocaine action.

PMID:
22910457
PMCID:
PMC3521972
DOI:
10.1038/npp.2012.154
[Indexed for MEDLINE]
Free PMC Article

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