Literature DB >> 32273471

Dopaminylation of histone H3 in ventral tegmental area regulates cocaine seeking.

Ashley E Lepack1, Craig T Werner2, Andrew F Stewart1, Sasha L Fulton1, Ping Zhong3, Lorna A Farrelly1, Alexander C W Smith1, Aarthi Ramakrishnan1, Yang Lyu1, Ryan M Bastle1, Jennifer A Martin2, Swarup Mitra2, Richard M O'Connor1, Zi-Jun Wang3, Henrik Molina4, Gustavo Turecki5, Li Shen1, Zhen Yan3, Erin S Calipari6, David M Dietz2, Paul J Kenny1, Ian Maze7,8.   

Abstract

Vulnerability to relapse during periods of attempted abstinence from cocaine use is hypothesized to result from the rewiring of brain reward circuitries, particularly ventral tegmental area (VTA) dopamine neurons. How cocaine exposures act on midbrain dopamine neurons to precipitate addiction-relevant changes in gene expression is unclear. We found that histone H3 glutamine 5 dopaminylation (H3Q5dop) plays a critical role in cocaine-induced transcriptional plasticity in the midbrain. Rats undergoing withdrawal from cocaine showed an accumulation of H3Q5dop in the VTA. By reducing H3Q5dop in the VTA during withdrawal, we reversed cocaine-mediated gene expression changes, attenuated dopamine release in the nucleus accumbens, and reduced cocaine-seeking behavior. These findings establish a neurotransmission-independent role for nuclear dopamine in relapse-related transcriptional plasticity in the VTA.
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

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Year:  2020        PMID： 32273471      PMCID： PMC7228137          DOI： 10.1126/science.aaw8806

Source DB:  PubMed          Journal:  Science        ISSN： 0036-8075            Impact factor:   47.728


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