Ethanol-induced sensitization depends preferentially on D-1 rather than D-2 dopamine receptors
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , , |
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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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:34652022-11-04T17:18:49Repositório 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 |
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info:eu-repo/semantics/article |
format |
article |
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 |
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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 |
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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 |
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eng |
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Pharmacology Biochemistry and Behavior |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy info:eu-repo/semantics/openAccess |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy |
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openAccess |
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173-180 |
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Elsevier B.V. |
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Elsevier B.V. |
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