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dc.contributor.authorCastino, MR
dc.contributor.authorBaker-Andresen, D
dc.contributor.authorRatnu, VS
dc.contributor.authorShevchenko, G
dc.contributor.authorMorris, KV
dc.contributor.authorBredy, TW
dc.contributor.authorYoungson, NA
dc.contributor.authorClemens, KJ
dc.date.accessioned2020-12-14T22:09:46Z
dc.date.available2020-12-14T22:09:46Z
dc.date.issued2018
dc.identifier.issn1601-1848
dc.identifier.doi10.1111/gbb.12421
dc.identifier.urihttp://hdl.handle.net/10072/400152
dc.description.abstractDrugs of addiction lead to a wide range of epigenetic changes at the promoter regions of genes directly implicated in learning and memory processes. We have previously shown that the histone deactylase inhibitor, sodium butyrate (NaB), accelerates the extinction of nicotine-seeking and provides resistance to relapse. Here, we explore the potential molecular mechanisms underlying this effect. Rats received intravenous nicotine or saline self-administration, followed by 6 days of extinction training, with each extinction session followed immediately by treatment with NaB or vehicle. On the last day of extinction, rats were killed and the medial ventral prefrontal cortex retained for chromatin immunoprecipitation and quantitative polymerase chain reaction (qPCR). A history of nicotine exposure significantly decreased H3K14 acetylation at the brain-derived neurotrophic factor (BDNF) exon IV promoter, and this effect was abolished with NaB treatment. In contrast, nicotine self-administration alone, resulted in a significant decrease in histone methylation at the H3K27me3 and H3K9me2 marks in the promoter regions of BDNF exon IV and cyclin-dependent kinase 5 (Cdk-5). Quantitative PCR-identified changes in several genes associated with NaB treatment that were independent of nicotine exposure; however, an interaction of nicotine history and NaB treatment was detected only in the expression of BDNF IV and BDNF IX. Together these results suggest that nicotine self-administration leads to a number of epigenetic changes at both the BDNF and Cdk-5 promoters, and that these changes may contribute to the enhanced extinction of nicotine-seeking by NaB.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherWiley
dc.relation.ispartofpagefrom98
dc.relation.ispartofpageto106
dc.relation.ispartofissue2
dc.relation.ispartofjournalGenes, Brain and Behavior
dc.relation.ispartofvolume17
dc.subject.fieldofresearchBiological sciences
dc.subject.fieldofresearchBiomedical and clinical sciences
dc.subject.fieldofresearchPsychology
dc.subject.fieldofresearchcode31
dc.subject.fieldofresearchcode32
dc.subject.fieldofresearchcode52
dc.subject.keywordsBDNF
dc.subject.keywordscdk-5
dc.subject.keywordsepigenetics
dc.subject.keywordshistone acetylation
dc.subject.keywordshistone methylation
dc.titlePersistent histone modifications at the BDNF and Cdk-5 promoters following extinction of nicotine-seeking in rats
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationCastino, MR; Baker-Andresen, D; Ratnu, VS; Shevchenko, G; Morris, KV; Bredy, TW; Youngson, NA; Clemens, KJ, Persistent histone modifications at the BDNF and Cdk-5 promoters following extinction of nicotine-seeking in rats, Genes, Brain and Behavior, 2018, 17 (2), pp. 98-106
dcterms.dateAccepted2017-08-25
dc.date.updated2020-12-10T04:12:15Z
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© 2018 Wiley Periodicals Inc. This is the peer reviewed version of the following article: PUBTITLE, Genes, Brain and Behavior, Volume 17, Issue 2, February 2018, Pages 98-106, which has been published in final form at 10.1111/gbb.12421. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving (http://olabout.wiley.com/WileyCDA/Section/id-828039.html)
gro.hasfulltextFull Text
gro.griffith.authorMorris, Kevin V.


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