Evidence map›Paper›PMID 28857504›Full record

ArticleGenes, brain, and behavior2018

Persistent histone modifications at the BDNF and Cdk-5 promoters following extinction of nicotine-seeking in rats.

M R Castino, D Baker-Andresen, V S Ratnu, G Shevchenko, K V Morris, T W Bredy, N A Youngson, K J Clemens

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, brain, and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

M R CastinoSchool of Psychology, University of New South Wales, Sydney, Australia.
D Baker-AndresenQueensland Brain Institute, The University of Queensland, Brisbane, Australia.
V S RatnuQueensland Brain Institute, The University of Queensland, Brisbane, Australia.
G ShevchenkoCenter for Gene Therapy, City of Hope, Duarte, CA, USA.
K V MorrisCenter for Gene Therapy, City of Hope, Duarte, CA, USA.
T W BredyQueensland Brain Institute, The University of Queensland, Brisbane, Australia.ORCID 0000-0003-3280-126X
N A YoungsonSchool of Medical Sciences, University of New South Wales, Sydney, Australia.
K J ClemensSchool of Psychology, University of New South Wales, Sydney, Australia.ORCID 0000-0003-2709-218X
The University of Queensland · AUUNSW Sydney · AUCity Of Hope National Medical Center · US

Funding

Transcriptional control, targeted modification, and excision of HIV in the brainR01MH113407 · NIMH · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI BURNETT, JOHN CORY · 2017 to 2021
$3.0M
Targeted inhibition of HIV-1 latencyR01AI111139 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI MORRIS, KEVIN V · 2014 to 2018
$2.7M
NIAID NIH HHS R01 AI111139NIMH NIH HHS R01 MH113407
6 · The paper itself

Abstract

Drugs 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.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorConditioning, OperantCyclin-Dependent Kinase 5Drug-Seeking BehaviorHistone CodeMaleMemoryNicotinePromoter Regions, GeneticRats, Sprague-DawleySelf AdministrationBrain-Derived Neurotrophic FactorCyclin-Dependent Kinase 5NicotineBDNFcdk-5epigeneticshistone acetylationhistone methylationnicotine

Identifiers

PMID28857504
PMCPMC5820208
OpenAlexW2752589867

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.