Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors

Detalhes bibliográficos
Autor(a) principal: Camarini, Rosana [UNIFESP]
Data de Publicação: 2011
Outros Autores: Marcourakis, Tania, Teodorov, Elizabeth, Yonamine, Mauricio, Calil, Helena Maria [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/33568
http://dx.doi.org/10.1016/j.pbb.2010.12.017
Resumo: Behavioral sensitization, defined as a progressive increase in the locomotor stimulant effects elicited by repeated exposure to drugs of abuse, has been used as an animal model for drug craving in humans. the mesoaccumbens dopaminergic system has been proposed to be critically involved in this phenomenon; however, few studies have been designed to systematically investigate the effects of dopaminergic antagonists on development and expression of behavioral sensitization to ethanol in Swiss mice. We first tested the effects of D-1 antagonist SCH-23390 (0-0.03 mg/kg) or D-2 antagonist Sulpiride (0-30 mg/kg) on the locomotor responses to an acute injection of ethanol (2.0 g/kg). Results showed that all tested doses of the antagonists were effective in blocking ethanol's stimulant effects. in another set of experiments, mice were pretreated intraperitoneally with SCH-23390 (0.01 mg/kg) or Sulpiride (10 mg/kg) 30 min before saline or ethanol injection, for 21 days. Locomotor activity was measured weekly for 20 min. Four days following this pretreatment, all mice were challenged with ethanol. Both antagonists attenuated the development of ethanol sensitization, but only SCH-23390 blocked the expression of ethanol sensitization according to this protocol. When we tested a single dose (30 min before tests) of either antagonist in mice treated chronically with ethanol, both antagonists attenuated ethanol-induced effects. the present findings demonstrate that the concomitant administration of ethanol with D-1 but not D-2 antagonist prevented the expression of ethanol sensitization, suggesting that the neuroadaptations underlying ethanol behavioral sensitization depend preferentially on D-1 receptor actions. (C) 2010 Elsevier Inc. All rights reserved.
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spelling Camarini, Rosana [UNIFESP]Marcourakis, TaniaTeodorov, ElizabethYonamine, MauricioCalil, Helena Maria [UNIFESP]Universidade de São Paulo (USP)Universidade Federal do ABC (UFABC)Universidade Federal de São Paulo (UNIFESP)2016-01-24T14:06:19Z2016-01-24T14:06:19Z2011-04-01Pharmacology Biochemistry and Behavior. Oxford: Pergamon-Elsevier B.V., v. 98, n. 2, p. 173-180, 2011.0091-3057http://repositorio.unifesp.br/handle/11600/33568http://dx.doi.org/10.1016/j.pbb.2010.12.017WOS000289396300002.pdf10.1016/j.pbb.2010.12.017WOS:000289396300002Behavioral sensitization, defined as a progressive increase in the locomotor stimulant effects elicited by repeated exposure to drugs of abuse, has been used as an animal model for drug craving in humans. the mesoaccumbens dopaminergic system has been proposed to be critically involved in this phenomenon; however, few studies have been designed to systematically investigate the effects of dopaminergic antagonists on development and expression of behavioral sensitization to ethanol in Swiss mice. We first tested the effects of D-1 antagonist SCH-23390 (0-0.03 mg/kg) or D-2 antagonist Sulpiride (0-30 mg/kg) on the locomotor responses to an acute injection of ethanol (2.0 g/kg). Results showed that all tested doses of the antagonists were effective in blocking ethanol's stimulant effects. in another set of experiments, mice were pretreated intraperitoneally with SCH-23390 (0.01 mg/kg) or Sulpiride (10 mg/kg) 30 min before saline or ethanol injection, for 21 days. Locomotor activity was measured weekly for 20 min. Four days following this pretreatment, all mice were challenged with ethanol. Both antagonists attenuated the development of ethanol sensitization, but only SCH-23390 blocked the expression of ethanol sensitization according to this protocol. When we tested a single dose (30 min before tests) of either antagonist in mice treated chronically with ethanol, both antagonists attenuated ethanol-induced effects. the present findings demonstrate that the concomitant administration of ethanol with D-1 but not D-2 antagonist prevented the expression of ethanol sensitization, suggesting that the neuroadaptations underlying ethanol behavioral sensitization depend preferentially on D-1 receptor actions. (C) 2010 Elsevier Inc. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Inst Ciencias Biomed, Dept Farmacol, BR-05508900 São Paulo, BrazilUniv São Paulo, Fac Ciencias Farmaceut, BR-05508900 São Paulo, BrazilUniv Fed ABC, Ctr Matemat Comp & Cognicao, Santo Andre, SP, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Psicobiol, São Paulo, BrazilWeb of Science173-180engElsevier B.V.Pharmacology Biochemistry and Behaviorhttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policyinfo:eu-repo/semantics/openAccessEthanolBehavioral sensitizationSCH-23390SulpirideDopamine receptor antagonistMiceEthanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptorsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000289396300002.pdfapplication/pdf417646${dspace.ui.url}/bitstream/11600/33568/1/WOS000289396300002.pdfdfa32b5708fba2d688787708a7821887MD51open accessTEXTWOS000289396300002.pdf.txtWOS000289396300002.pdf.txtExtracted texttext/plain55047${dspace.ui.url}/bitstream/11600/33568/2/WOS000289396300002.pdf.txt2e78eaecc088ce530068d0a10077fb98MD52open access11600/335682022-11-04 14:18:49.566open accessoai:repositorio.unifesp.br:11600/33568Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:28:42.384077Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
title Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
spellingShingle Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
Camarini, Rosana [UNIFESP]
Ethanol
Behavioral sensitization
SCH-23390
Sulpiride
Dopamine receptor antagonist
Mice
title_short Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
title_full Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
title_fullStr Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
title_full_unstemmed Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
title_sort Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
author Camarini, Rosana [UNIFESP]
author_facet Camarini, Rosana [UNIFESP]
Marcourakis, Tania
Teodorov, Elizabeth
Yonamine, Mauricio
Calil, Helena Maria [UNIFESP]
author_role author
author2 Marcourakis, Tania
Teodorov, Elizabeth
Yonamine, Mauricio
Calil, Helena Maria [UNIFESP]
author2_role author
author
author
author
dc.contributor.institution.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Federal do ABC (UFABC)
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Camarini, Rosana [UNIFESP]
Marcourakis, Tania
Teodorov, Elizabeth
Yonamine, Mauricio
Calil, Helena Maria [UNIFESP]
dc.subject.eng.fl_str_mv Ethanol
Behavioral sensitization
SCH-23390
Sulpiride
Dopamine receptor antagonist
Mice
topic Ethanol
Behavioral sensitization
SCH-23390
Sulpiride
Dopamine receptor antagonist
Mice
description Behavioral sensitization, defined as a progressive increase in the locomotor stimulant effects elicited by repeated exposure to drugs of abuse, has been used as an animal model for drug craving in humans. the mesoaccumbens dopaminergic system has been proposed to be critically involved in this phenomenon; however, few studies have been designed to systematically investigate the effects of dopaminergic antagonists on development and expression of behavioral sensitization to ethanol in Swiss mice. We first tested the effects of D-1 antagonist SCH-23390 (0-0.03 mg/kg) or D-2 antagonist Sulpiride (0-30 mg/kg) on the locomotor responses to an acute injection of ethanol (2.0 g/kg). Results showed that all tested doses of the antagonists were effective in blocking ethanol's stimulant effects. in another set of experiments, mice were pretreated intraperitoneally with SCH-23390 (0.01 mg/kg) or Sulpiride (10 mg/kg) 30 min before saline or ethanol injection, for 21 days. Locomotor activity was measured weekly for 20 min. Four days following this pretreatment, all mice were challenged with ethanol. Both antagonists attenuated the development of ethanol sensitization, but only SCH-23390 blocked the expression of ethanol sensitization according to this protocol. When we tested a single dose (30 min before tests) of either antagonist in mice treated chronically with ethanol, both antagonists attenuated ethanol-induced effects. the present findings demonstrate that the concomitant administration of ethanol with D-1 but not D-2 antagonist prevented the expression of ethanol sensitization, suggesting that the neuroadaptations underlying ethanol behavioral sensitization depend preferentially on D-1 receptor actions. (C) 2010 Elsevier Inc. All rights reserved.
publishDate 2011
dc.date.issued.fl_str_mv 2011-04-01
dc.date.accessioned.fl_str_mv 2016-01-24T14:06:19Z
dc.date.available.fl_str_mv 2016-01-24T14:06:19Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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status_str publishedVersion
dc.identifier.citation.fl_str_mv Pharmacology Biochemistry and Behavior. Oxford: Pergamon-Elsevier B.V., v. 98, n. 2, p. 173-180, 2011.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/33568
http://dx.doi.org/10.1016/j.pbb.2010.12.017
dc.identifier.issn.none.fl_str_mv 0091-3057
dc.identifier.file.none.fl_str_mv WOS000289396300002.pdf
dc.identifier.doi.none.fl_str_mv 10.1016/j.pbb.2010.12.017
dc.identifier.wos.none.fl_str_mv WOS:000289396300002
identifier_str_mv Pharmacology Biochemistry and Behavior. Oxford: Pergamon-Elsevier B.V., v. 98, n. 2, p. 173-180, 2011.
0091-3057
WOS000289396300002.pdf
10.1016/j.pbb.2010.12.017
WOS:000289396300002
url http://repositorio.unifesp.br/handle/11600/33568
http://dx.doi.org/10.1016/j.pbb.2010.12.017
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Pharmacology Biochemistry and Behavior
dc.rights.driver.fl_str_mv http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 173-180
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
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