HDAC inhibitors reverse mania-like behavior and modulate epigenetic regulatory enzymes in an animal model of mania induced by Ouabain.


Journal

Pharmacology, biochemistry, and behavior
ISSN: 1873-5177
Titre abrégé: Pharmacol Biochem Behav
Pays: United States
ID NLM: 0367050

Informations de publication

Date de publication:
06 2020
Historique:
received: 29 11 2019
revised: 23 03 2020
accepted: 24 03 2020
pubmed: 31 3 2020
medline: 22 1 2021
entrez: 31 3 2020
Statut: ppublish

Résumé

The etiology of bipolar disorder (BD) is multifactorial, involving both environmental and genetic factors. Current pharmacological treatment is associated with several side effects, which are the main reason patients discontinue treatment. Epigenetic alterations have been studied for their role in the pathophysiology of BD, as they bridge the gap between gene and environment. Evaluate the effects of histone deacetylase inhibitors on behavior and epigenetic enzymes activity in a rat model of mania induced by ouabain. Adult male rats were subjected to a single intracerebroventricular injection of ouabain (10 Ouabain induced hyperactivity in rats, which was reversed by valproate and sodium butyrate treatment. Ouabain did not alter the activity of any of the enzymes evaluated. However, valproate and sodium butyrate decreased the activity of histone deacetylase and DNA methyltransferase. Moreover, there was a positive correlation between these two enzymes. These results suggest that targeting epigenetic mechanisms may play an important role in mania-like behavior management.

Sections du résumé

BACKGROUND
The etiology of bipolar disorder (BD) is multifactorial, involving both environmental and genetic factors. Current pharmacological treatment is associated with several side effects, which are the main reason patients discontinue treatment. Epigenetic alterations have been studied for their role in the pathophysiology of BD, as they bridge the gap between gene and environment.
OBJECTIVE
Evaluate the effects of histone deacetylase inhibitors on behavior and epigenetic enzymes activity in a rat model of mania induced by ouabain.
METHODS
Adult male rats were subjected to a single intracerebroventricular injection of ouabain (10
RESULTS
Ouabain induced hyperactivity in rats, which was reversed by valproate and sodium butyrate treatment. Ouabain did not alter the activity of any of the enzymes evaluated. However, valproate and sodium butyrate decreased the activity of histone deacetylase and DNA methyltransferase. Moreover, there was a positive correlation between these two enzymes.
CONCLUSION
These results suggest that targeting epigenetic mechanisms may play an important role in mania-like behavior management.

Identifiants

pubmed: 32222371
pii: S0091-3057(19)30587-8
doi: 10.1016/j.pbb.2020.172917
pii:
doi:

Substances chimiques

Histone Deacetylase Inhibitors 0
Butyric Acid 107-92-6
Ouabain 5ACL011P69
Valproic Acid 614OI1Z5WI
DNA (Cytosine-5-)-Methyltransferases EC 2.1.1.37
Histone Acetyltransferases EC 2.3.1.48
Histone Deacetylases EC 3.5.1.98

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

172917

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest JQ has the following declarations of interest: Clinical Research Support: Janssen Pharmaceutical (Clinical Trial), Allergan (Clinical Trial); Advisory Boards, Speaker Bureaus, Expert Witness, or Consultant: Daiichi Sankyo (Speaker Bureau); Patent, Equity, or Royalty: Instituto de Neurociencias Dr. Joao Quevedo (Stockholder); Other: Artmed Editora (Copyright), Artmed Panamericana (Copyright). All the other authors have no conflict of interest.

Auteurs

Roger B Varela (RB)

Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia; Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil.

Wilson R Resende (WR)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil.

Gustavo C Dal-Pont (GC)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil.

Fernanda F Gava (FF)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil.

Susannah J Tye (SJ)

Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia; Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA.

João Quevedo (J)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil; Translational Psychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth) -, Houston, TX, USA; Center of Excellence on Mood Disorders, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth) -, Houston, TX, USA; Neuroscience Graduate Program, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences -, Houston, TX, USA.

Samira S Valvassori (SS)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) -, Criciúma, SC, Brazil. Electronic address: samiravalvassori@unesc.net.

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Classifications MeSH