Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition
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Altres documents de l'autoria: Sanchis-Segura, Carla; López Atalaya, José P.; Barco, Ángel
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Mostra el registre complet de l'elementcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/8033
comunitat-uji-handle3:10234/8636
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INVESTIGACIONMetadades
Títol
Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase InhibitionData de publicació
2009Editor
Nature Publishing GroupISSN
0893-133XTipus de document
info:eu-repo/semantics/articleVersió de l'editorial
http://www.nature.com/npp/journal/v34/n13/abs/npp2009125a.htmlVersió
info:eu-repo/semantics/submittedVersionParaules clau / Matèries
Resum
Histone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Earlier studies have shown that ... [+]
Histone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Earlier studies have shown that a reduction in histone deacetylase (HDAC) activity results in the enhancement of some psychostimulant-induced behaviors. In this study, we extend those seminal findings by showing that the administration of the HDAC inhibitor sodium butyrate enhances morphine-induced locomotor sensitization and conditioned place preference. In contrast, this compound has no effects on the development of morphine tolerance and dependence. Similar effects were observed for cocaine and ethanol-induced behaviors. These behavioral changes were accompanied by a selective boosting of a component of the transcriptional program activated by chronic morphine administration that included circadian clock genes and other genes relevant to addictive behavior. Our results support a specific function for histone acetylation and the epigenetic modulation of transcription at a reduced number of biologically relevant loci on non-homeostatic, long-lasting, drug-induced behavioral plasticity. [-]
Publicat a
Neuropsychopharmacology, 34, p. 2642–2654Drets d'accés
http://rightsstatements.org/vocab/CNE/1.0/
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/openAccess
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