ArticleThe international journal of neuropsychopharmacology2014
Effects of histone deacetylase inhibitors on amygdaloid histone acetylation and neuropeptide Y expression: a role in anxiety-like and alcohol-drinking behaviours.
Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 86 citations in OpenAlex.
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- Mechanisms of aerobic exercise effects on the gut microbiota and its metabolites in anxiety disorders.Frontiers in microbiology · 2025Review
- Epigenetic drugs and psychedelics as emerging therapies for alcohol use disorder: insights from preclinical studies.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
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- Effects of entinostat, quisinostat, and tubastatin-A on alcohol consumption in male high ethanol consuming rats.Frontiers in epigenetics and epigenomics · 2024Article
- The role of epigenetics in anxiety disorders.Molecular biology reports · 2023Review
- A Role for Histone Deacetylases in the Biology and Treatment of Post-Traumatic Stress Disorder: What Do We Know and Where Do We Go from Here?Complex psychiatry · 2022Review
- Epigenetic Effects of Addictive Drugs in the Nucleus Accumbens.Frontiers in molecular neuroscience · 2022Review
- Acute and Protracted Prenatal Stress Produce Mood Disorder-Like and Ethanol Drinking Behaviors in Male and Female Adult Offspring.Frontiers in behavioral neuroscience · 2022Article
- Targeting Epigenetic Mechanisms to Treat Alcohol Use Disorders (AUD).Current pharmaceutical design · 2021Article
- CB1 receptor neutral antagonist treatment epigenetically increases neuropeptide Y expression and decreases alcohol drinking.Neuropharmacology · 2021Article
- Integration of peripheral transcriptomics, genomics, and interactomics following trauma identifies causal genes for symptoms of post-traumatic stress and major depression.Molecular psychiatry · 2021Observational
- Histone modifications, DNA methylation, and the epigenetic code of alcohol use disorder.International review of neurobiology · 2021Article
- Epigenetic mechanisms underlying pathobiology of alcohol use disorder.Current pathobiology reports · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies have demonstrated the involvement of epigenetic mechanisms in psychiatric disorders, including alcoholism. Here, we investigated the effects of histone deacetylase (HDAC) inhibitor, trichostatin A (TSA) on amygdaloid HDAC-induced histone deacetylation and neuropeptide Y (NPY) expression and on anxiety-like and alcohol-drinking behaviours in alcohol-preferring (P) and -non-preferring (NP) rats. It was found that P rats displayed higher anxiety-like and alcohol-drinking behaviours, higher amygdaloid nuclear, but not cytosolic, HDAC activity, which was associated with increased HDAC2 protein levels and deficits in histone acetylation and NPY expression in the central (CeA) and medial nucleus of amygdala (MeA), as compared to NP rats. TSA treatment attenuated the anxiety-like and alcohol-drinking behaviours, with concomitant reductions in amygdaloid nuclear, but not cytosolic HDAC activity, and HDAC2, but not HDAC4, protein levels in the CeA and MeA of P rats, without effect in NP rats. TSA treatment also increased global histone acetylation (H3-K9 and H4-K8) and NPY expression in the CeA and MeA of P, but not in NP rats. Histone H3 acetylation within the NPY promoter was also innately lower in the amygdala of P rats compared with NP rats; which was normalized by TSA treatment. Voluntary ethanol intake in P, but not NP rats, produced anxiolytic effects and decreased the HDAC2 levels and increased histone acetylation in the CeA and MeA. These results suggest that higher HDAC2 expression-related deficits in histone acetylation may be involved in lower NPY expression in the amygdala of P rats, and operative in controlling anxiety-like and alcohol-drinking behaviours.
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