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http://hdl.handle.net/10261/59577
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dc.contributor.author | Bilbao, Ainhoa | - |
dc.contributor.author | Cippitelli, Andrea | - |
dc.contributor.author | Martín- Hernández, A. B. | - |
dc.contributor.author | Granado, Noelia | - |
dc.contributor.author | Ortiz, Óscar | - |
dc.contributor.author | Bezard, Erwan | - |
dc.contributor.author | Chen, Jiang-Fan | - |
dc.contributor.author | Navarro, Miguel | - |
dc.contributor.author | Rodríguez de Fonseca, Fernando | - |
dc.contributor.author | Moratalla, Rosario | - |
dc.date.accessioned | 2012-11-06T13:09:54Z | - |
dc.date.available | 2012-11-06T13:09:54Z | - |
dc.date.issued | 2006 | - |
dc.identifier | doi: 10.1007/s00213-005-0284-0 | - |
dc.identifier | issn: 0033-3158 | - |
dc.identifier.citation | Psychopharmacology 185: 160- 168 (2006) | - |
dc.identifier.uri | http://hdl.handle.net/10261/59577 | - |
dc.description.abstract | Rationale: Caffeine and other methylxanthines induce behavioral activation and anxiety responses in mice via antagonist action at A2A adenosine receptors. When combined with the opioid antagonist naloxone, methylxanthines produce a characteristic quasi-morphine withdrawal syndrome (QMWS) in opiate-naive animals. Objectives: The aim of this study was to establish the role of A2A receptors in the quasi-morphine withdrawal syndrome induced by co-administration of caffeine and naloxone and in the behavioral effects of caffeine. Methods: We have used A2A receptor knockout (A2AR-/-) mice in comparison with their wild-type and heterozygous littermates to measure locomotor activity in the open field and withdrawal symptoms induced by caffeine and naloxone. Naïve wild-type and knockout mice were also examined for enkephalin and dynorphin mRNA expression by in situ hybridization and for μ-opiate receptor by ligand binding autoradiography to check for possible opiate receptor changes induced by A 2A receptor inactivation. Results: Caffeine increases locomotion and anxiety in wild-type animals, but it has no psychomotor effects in A 2AR-/- mice. Co-administration of caffeine (20 mg/kg) and naloxone (2 mg/kg) resulted in a severe quasi-morphine withdrawal syndrome in wild-type mice that was almost completely abolished in A2AR -/- mice. Heterozygous animals exhibited a 40% reduction in withdrawal symptoms, suggesting that there is no genetic/developmental compensation for the inactivation of one of the A2AR alleles. A 2AR-/- and wild-type mice have similar levels of striatal μ-opioid receptors, thus the effect is not due to altered opioid receptor expression. Conclusions: Our results demonstrate that A2A receptors are required for the induction of quasi-morphine withdrawal syndrome by co-administration of caffeine and naloxone and implicate striatal A2A receptors and μ-opiate receptors in tonic inhibition of motor activity in the striatum. © Springer-Verlag 2006. | - |
dc.language.iso | eng | - |
dc.publisher | Springer Nature | - |
dc.rights | closedAccess | - |
dc.title | Absence of quasi-morphine withdrawal syndrome in adenosine A2A receptor knockout mice | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1007/s00213-005-0284-0 | - |
dc.date.updated | 2012-11-06T13:09:54Z | - |
dc.description.version | Peer Reviewed | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.languageiso639-1 | en | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | none | - |
item.openairetype | artículo | - |
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