Essential Role of the Histone Methyltransferase G9a in Cocaine-Induced Plasticity
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Cocaine Addiction and Histone Methylation: Long-lasting behavioral syndromes associated with chronic cocaine exposure may result from dysregulation of the global transcriptional machinery. Maze et al. (p. 213 ) observed that histone lysine methylation in the nucleus accumbens plays a critical role in mediating the regulation of gene expression in response to repeated cocaine self-administration. Chronic cocaine was linked to overall reductions in dimethylation of lysine 9 of histone 3 (H3K9) in this brain region. Repressing H3K9 after chronic cocaine administration facilitated reward-related changes in behavior. The authors identifed the methyltransferase G9a as an essential mediator and an important regulator of dendritic spine plasticity. Downregulation of G9a was linked to the transcription factor ΔFosB.
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Manipulation of enzymes that control histone acetylation or deacetylation or DNA methylation in the nucleus accumbens modifies drug behavioral responses, supporting their relevance to drug reward and SUDs.
“Moreover, the manipulation of enzymes that control histone acetylation or deacetylation or DNA methylation in the nucleus accumbens modifies drug behavioral responses, supporting their relevance to drug reward and SUDs 111,112 .”
From Substance use disorders: a comprehensive update of classification, epidemiology, neurobiology, clinical aspects, treatment and prevention (2023) · cites this paper as [111]
The paper reports that manipulating G9a in the nucleus accumbens changes cocaine preference (passage 5, section labeled Abstract). But G9a controls histone methylation, not histone acetylation, deacetylation, or DNA methylation. The paper mentions histone acetylation as background (passage 1), without showing the enzyme manipulations specified in the claim. (LLM, conf=0.84)
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- Authors
- Maze, I., Covington, H. E., Dietz, D. M., LaPlant, Q., Renthal, W., Russo, S. J., Mechanic, M., Mouzon, E., Neve, R. L., Haggarty, S. J., Ren, Y., Sampath, S. C., Hurd, Y. L., Greengard, P., Tarakhovsky, A., Schaefer, A., & Nestler, E. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- The University of Texas Southwestern Medical Center (US)
- Massachusetts Institute of Technology (US)
- Broad Institute (US)
- Rockefeller University (US)
- ORCID
- Venue
- Science
- Published
- 2010-01-08
- Volume
- 327
- Issue
- 5962
- Pages
- 213-216
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2820240
- OpenAlex
- W2022851859
- Cited by
- 665
- References
- 27
- Citations by year
- 2026: 6 · 2025: 16 · 2024: 26 · 2023: 23 · 2022: 29 · 2021: 43 · 2020: 32 · 2019: 45 · 2018: 41 · 2017: 47 · 2016: 56 · 2015: 45 · 2014: 54 · 2013: 52 · 2012: 59
- FWCI
- 26.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Public Health Service (P0110044)
- National Institute on Drug Abuse (P01DA010044, P01DA008227, R01DA007359, R01DA014133)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- G9a, histone methyltransferase, H3K9 dimethylation, cocaine, cocaine dependence, nucleus accumbens, ΔFosB, dendritic spine plasticity, synaptic plasticity, epigenetic regulation, gene expression
- MeSH terms
- Animals, Behavior, Animal, Cocaine, Enzyme Repression, Gene Expression Regulation, Histones, Lysine, Male, Methylation, Mice, Inbred C57BL, Neuronal Plasticity, Neurons, Nucleus Accumbens, Histone-Lysine N-Methyltransferase, Reward, Self Administration, Transcription, Genetic, Down-Regulation, Proto-Oncogene Proteins c-fos, Cocaine-Related Disorders, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Dendritic Spines, Mice
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