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Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish

Nicotine induces long-term changes in the neural activity of the mesocorticolimbic reward pathway structures. The mechanisms involved in this process have not been fully characterized. The hypothesis discussed here proposed that epigenetic regulation participates in the installation of persistent ad...

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Autores principales: Faillace, Maria P., Bernabeu, Ramón O.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9608226/
https://www.ncbi.nlm.nih.gov/pubmed/34279203
http://dx.doi.org/10.2174/1570159X19666210716112351
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author Faillace, Maria P.
Bernabeu, Ramón O.
author_facet Faillace, Maria P.
Bernabeu, Ramón O.
author_sort Faillace, Maria P.
collection PubMed
description Nicotine induces long-term changes in the neural activity of the mesocorticolimbic reward pathway structures. The mechanisms involved in this process have not been fully characterized. The hypothesis discussed here proposed that epigenetic regulation participates in the installation of persistent adaptations and long-lasting synaptic plasticity generated by nicotine action on the mesolimbic dopamine neurons of zebrafish. The epigenetic mechanisms induced by nicotine entail histone and DNA chemical modifications, which have been described to lead to changes in gene expression. Among the enzymes that catalyze epigenetic chemical modifications, histone deacetylases (HDACs) remove acetyl groups from histones, thereby facilitating DNA relaxation and making DNA more accessible to gene transcription. DNA methylation, which is dependent on DNA methyltransferase (DNMTs) activity, inhibits gene expression by recruiting several methyl binding proteins that prevent RNA polymerase binding to DNA. In zebrafish, phenylbutyrate (PhB), an HDAC inhibitor, abolishes nicotine rewarding properties together with a series of typical reward-associated behaviors. Furthermore, PhB and nicotine alter long- and short-term object recognition memory in zebrafish, respectively. Regarding DNA methylation effects, a methyl group donor L-methionine (L-met) was found to dramatically reduce nicotine-induced conditioned place preference (CPP) in zebrafish. Simultaneous treatment with DNMT inhibitor 5-aza-2’-deoxycytidine (AZA) was found to reverse the L-met effect on nicotine-induced CPP as well as nicotine reward-specific effects on genetic expression in zebrafish. Therefore, pharmacological interventions that modulate epigenetic regulation of gene expression should be considered as a potential therapeutic method to treat nicotine addiction.
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spelling pubmed-96082262022-11-07 Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish Faillace, Maria P. Bernabeu, Ramón O. Curr Neuropharmacol Neurology Nicotine induces long-term changes in the neural activity of the mesocorticolimbic reward pathway structures. The mechanisms involved in this process have not been fully characterized. The hypothesis discussed here proposed that epigenetic regulation participates in the installation of persistent adaptations and long-lasting synaptic plasticity generated by nicotine action on the mesolimbic dopamine neurons of zebrafish. The epigenetic mechanisms induced by nicotine entail histone and DNA chemical modifications, which have been described to lead to changes in gene expression. Among the enzymes that catalyze epigenetic chemical modifications, histone deacetylases (HDACs) remove acetyl groups from histones, thereby facilitating DNA relaxation and making DNA more accessible to gene transcription. DNA methylation, which is dependent on DNA methyltransferase (DNMTs) activity, inhibits gene expression by recruiting several methyl binding proteins that prevent RNA polymerase binding to DNA. In zebrafish, phenylbutyrate (PhB), an HDAC inhibitor, abolishes nicotine rewarding properties together with a series of typical reward-associated behaviors. Furthermore, PhB and nicotine alter long- and short-term object recognition memory in zebrafish, respectively. Regarding DNA methylation effects, a methyl group donor L-methionine (L-met) was found to dramatically reduce nicotine-induced conditioned place preference (CPP) in zebrafish. Simultaneous treatment with DNMT inhibitor 5-aza-2’-deoxycytidine (AZA) was found to reverse the L-met effect on nicotine-induced CPP as well as nicotine reward-specific effects on genetic expression in zebrafish. Therefore, pharmacological interventions that modulate epigenetic regulation of gene expression should be considered as a potential therapeutic method to treat nicotine addiction. Bentham Science Publishers 2022-03-04 2022-03-04 /pmc/articles/PMC9608226/ /pubmed/34279203 http://dx.doi.org/10.2174/1570159X19666210716112351 Text en © 2022 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/ This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Neurology
Faillace, Maria P.
Bernabeu, Ramón O.
Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title_full Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title_fullStr Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title_full_unstemmed Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title_short Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish
title_sort epigenetic mechanisms mediate nicotine-induced reward and behaviour in zebrafish
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9608226/
https://www.ncbi.nlm.nih.gov/pubmed/34279203
http://dx.doi.org/10.2174/1570159X19666210716112351
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