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Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus

SATB2 is a DNA binding protein that specifically binds the nuclear matrix attachment region and functions as a regulator of the transcription of large chromatin domains. Unlike its well addressed role during brain development, the role of SATB2 in adult brain is under-investigated. It has been shown...

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Autores principales: Salti, Ahmad, Apostolova, Galina, Kummer, Kai K., Lemos, Cristina, Dechant, Georg, El Rawas, Rana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6190852/
https://www.ncbi.nlm.nih.gov/pubmed/30356831
http://dx.doi.org/10.3389/fnbeh.2018.00224
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author Salti, Ahmad
Apostolova, Galina
Kummer, Kai K.
Lemos, Cristina
Dechant, Georg
El Rawas, Rana
author_facet Salti, Ahmad
Apostolova, Galina
Kummer, Kai K.
Lemos, Cristina
Dechant, Georg
El Rawas, Rana
author_sort Salti, Ahmad
collection PubMed
description SATB2 is a DNA binding protein that specifically binds the nuclear matrix attachment region and functions as a regulator of the transcription of large chromatin domains. Unlike its well addressed role during brain development, the role of SATB2 in adult brain is under-investigated. It has been shown that deletion of SATB2 from the forebrain of adult mice significantly impaired long-term memory for contextual fear and object recognition memory. The aim of the present study was to investigate the effects of appetitive stimuli such as cocaine and social interaction (SI) on SATB2 expression in the adult rat brain. For that, we performed conditioned place preference (CPP) to cocaine (15 mg/kg) and to SI, then assessed SATB2 expression in the brain 1 h (24 h after the last conditioning) and 24 h (48 h after the last conditioning) after the CPP test. We found that SATB2 expression in the paraventricular thalamus of rats was increased 1 h after the cocaine CPP test. This increase was selective for the cocaine-paired environment since the SI-paired environment did not increase SATB2 expression in the paraventricular thalamus. Also, the cocaine paired environment-induced increase of SATB2 levels in the paraventricular thalamus was due to cocaine conditioning as the unpaired cocaine group did not show an increase of SATB2 in the paraventricular thalamus. These results suggest that SATB2 in the paraventricular thalamus appears to be involved in the association between cocaine effects and environmental context. Further studies are needed to address the functional role of SATB2 in cocaine conditioning.
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spelling pubmed-61908522018-10-23 Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus Salti, Ahmad Apostolova, Galina Kummer, Kai K. Lemos, Cristina Dechant, Georg El Rawas, Rana Front Behav Neurosci Neuroscience SATB2 is a DNA binding protein that specifically binds the nuclear matrix attachment region and functions as a regulator of the transcription of large chromatin domains. Unlike its well addressed role during brain development, the role of SATB2 in adult brain is under-investigated. It has been shown that deletion of SATB2 from the forebrain of adult mice significantly impaired long-term memory for contextual fear and object recognition memory. The aim of the present study was to investigate the effects of appetitive stimuli such as cocaine and social interaction (SI) on SATB2 expression in the adult rat brain. For that, we performed conditioned place preference (CPP) to cocaine (15 mg/kg) and to SI, then assessed SATB2 expression in the brain 1 h (24 h after the last conditioning) and 24 h (48 h after the last conditioning) after the CPP test. We found that SATB2 expression in the paraventricular thalamus of rats was increased 1 h after the cocaine CPP test. This increase was selective for the cocaine-paired environment since the SI-paired environment did not increase SATB2 expression in the paraventricular thalamus. Also, the cocaine paired environment-induced increase of SATB2 levels in the paraventricular thalamus was due to cocaine conditioning as the unpaired cocaine group did not show an increase of SATB2 in the paraventricular thalamus. These results suggest that SATB2 in the paraventricular thalamus appears to be involved in the association between cocaine effects and environmental context. Further studies are needed to address the functional role of SATB2 in cocaine conditioning. Frontiers Media S.A. 2018-10-02 /pmc/articles/PMC6190852/ /pubmed/30356831 http://dx.doi.org/10.3389/fnbeh.2018.00224 Text en Copyright © 2018 Salti, Apostolova, Kummer, Lemos, Dechant and El Rawas. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Salti, Ahmad
Apostolova, Galina
Kummer, Kai K.
Lemos, Cristina
Dechant, Georg
El Rawas, Rana
Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title_full Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title_fullStr Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title_full_unstemmed Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title_short Cocaine Paired Environment Increases SATB2 Levels in the Rat Paraventricular Thalamus
title_sort cocaine paired environment increases satb2 levels in the rat paraventricular thalamus
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6190852/
https://www.ncbi.nlm.nih.gov/pubmed/30356831
http://dx.doi.org/10.3389/fnbeh.2018.00224
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