CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum

Remodeling chromatin is essential for cAMP-regulated gene expression, necessary not only for development but also for memory storage and other enduring mental states. Histone acetylation and deacetylation mediate long-lasting forms of synaptic plasticity in Aplysia as well as cognition in mice. Here...

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Main Authors: Levine, Amir A., Guan, Zhonghui, Barco, Angel, Xu, Shiqin, Kandel, Eric R., Schwartz, James H.
Formato: Artigo
Idioma:English
Publicado em: National Academy of Sciences 2005
Assuntos:
Biological Sciences
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC1323217/
https://ncbi.nlm.nih.gov/pubmed/16380431
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0509735102
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spelling pubmed-13232172006-06-27 CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum Levine, Amir A. Guan, Zhonghui Barco, Angel Xu, Shiqin Kandel, Eric R. Schwartz, James H. Proc Natl Acad Sci U S A Biological Sciences Remodeling chromatin is essential for cAMP-regulated gene expression, necessary not only for development but also for memory storage and other enduring mental states. Histone acetylation and deacetylation mediate long-lasting forms of synaptic plasticity in Aplysia as well as cognition in mice. Here, we show that histone acetylation by the cAMP-response element binding protein (CREB)-binding protein (CBP) mediates sensitivity to cocaine by regulating expression of the fosB gene and its splice variant, ΔfosB, a transcription factor previously implicated in addiction. Using the chromatin immunoprecipitation assay with antibodies against histone H4 or CBP, we find that CBP is recruited to the fosB promoter to acetylate histone H4 in response to acute exposure to cocaine. We show that mutant mice that lack one allele of the CBP gene and have normal levels of fosB expression are less sensitive to chronic (10-day) administration of cocaine than are wild-type mice. This decreased sensitivity is correlated with decreased histone acetylation and results in decreased fosB expression and diminished accumulation of ΔfosB. Thus, CBP, which forms part of the promoter complex with CREB, mediates sensitivity to cocaine by acetylating histones. National Academy of Sciences 2005-12-27 /pmc/articles/PMC1323217/ /pubmed/16380431 http://dx.doi.org/10.1073/pnas.0509735102 Text en Copyright © 2005, The National Academy of Sciences
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Biological Sciences
spellingShingle Biological Sciences
Levine, Amir A.
Guan, Zhonghui
Barco, Angel
Xu, Shiqin
Kandel, Eric R.
Schwartz, James H.
CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
description Remodeling chromatin is essential for cAMP-regulated gene expression, necessary not only for development but also for memory storage and other enduring mental states. Histone acetylation and deacetylation mediate long-lasting forms of synaptic plasticity in Aplysia as well as cognition in mice. Here, we show that histone acetylation by the cAMP-response element binding protein (CREB)-binding protein (CBP) mediates sensitivity to cocaine by regulating expression of the fosB gene and its splice variant, ΔfosB, a transcription factor previously implicated in addiction. Using the chromatin immunoprecipitation assay with antibodies against histone H4 or CBP, we find that CBP is recruited to the fosB promoter to acetylate histone H4 in response to acute exposure to cocaine. We show that mutant mice that lack one allele of the CBP gene and have normal levels of fosB expression are less sensitive to chronic (10-day) administration of cocaine than are wild-type mice. This decreased sensitivity is correlated with decreased histone acetylation and results in decreased fosB expression and diminished accumulation of ΔfosB. Thus, CBP, which forms part of the promoter complex with CREB, mediates sensitivity to cocaine by acetylating histones.
author Levine, Amir A.
Guan, Zhonghui
Barco, Angel
Xu, Shiqin
Kandel, Eric R.
Schwartz, James H.
author_facet Levine, Amir A.
Guan, Zhonghui
Barco, Angel
Xu, Shiqin
Kandel, Eric R.
Schwartz, James H.
author_sort Levine, Amir A.
title CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
title_short CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
title_full CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
title_fullStr CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
title_full_unstemmed CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum
title_sort creb-binding protein controls response to cocaine by acetylating histones at the fosb promoter in the mouse striatum
publisher National Academy of Sciences
publisher_facet National Academy of Sciences
publishDate 2005
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1323217/
https://ncbi.nlm.nih.gov/pubmed/16380431
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0509735102
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