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Pharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat.

dc.contributor.authorBlanco-Calvo, Eduardo
dc.contributor.authorRivera, Patricia
dc.contributor.authorArrabal, Sergio
dc.contributor.authorVargas, Antonio
dc.contributor.authorPavón, Francisco Javier
dc.contributor.authorSerrano, Antonia
dc.contributor.authorCastilla-Ortega, Estela
dc.contributor.authorGaleano, Pablo
dc.contributor.authorRubio, Leticia
dc.contributor.authorSuárez, Juan
dc.contributor.authorRodriguez de Fonseca, Fernando
dc.contributor.authoraffiliation[Blanco-Calvo,E] Departament de Pedagogia i Psicologia, Facultat de Ciències de l’Educació, Universitat de Lleida, Lleida, Spain. [Blanco-Calvo,E; Rivera,P; Arrabal,S; Vargas,A; Pavón,FJ; Serrano,A; Castilla-Ortega,E; Rodríguez de Fonseca,F] Laboratorio de Investigación-UGC de Salud Mental, Instituto de Investigación Biomédica de Málaga, Universidad de Málaga, Hospital Regional Universitario de Málaga, Málaga, Spain. [Galeano,P] Instituto de Investigaciones Cardiológicas Prof. Dr. Alberto C. Taquini, Universidad de Buenos Aires-CONICET, Ciudad de Buenos Aires, Argentina. [Rubio,L] Departamento de Anatomía y Medicina Legal y Forense, Facultad de Medicina, Universidad de Málaga, Málaga, Spain.es
dc.contributor.funderThe 7th Framework Program of the European Union [grant number HEALTH-F2-2008-223713, REPROBESITY], the Ministerio de Ciencia e Innovación [grant numbers SAF2010-19087, SAF 2010-20521], the Instituto de Salud Carlos III, the Ministerio de Economía y Competitividad, UE-ERDF [grant number CP12/03109], the Red de Trastornos Adictivos [grant numbers RD12/0028/0001, RD12/0028/0009], the CIBERobn, the Plan Nacional Sobre Drogas, Ministerio de Sanidad y Consumo [grant number PNSD 2010/143], the Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, the UE/ERDF [grant number CTS-433, P-11-CVI-07637], the Consejería de Salud, Junta de Andalucía [grant numbers PI0232/2008, PI0029/2008, SAS111224], and the Fundació La Marató de TV3 [grant number 386/C/2011]. JS is a recipient of a “Miguel Servet” research contract from the National System of Health (Instituto de Salud Carlos III, grant number CP12/03109). ECO is a recipient of a “Sara Borrell” research contract from the National System of Health (Instituto de Salud Carlos III, grant number CD12/00455).
dc.date.accessioned2014-05-28T12:44:20Z
dc.date.available2014-05-28T12:44:20Z
dc.date.issued2014-01-08
dc.descriptionJournal Article;es
dc.description.abstractAddiction to major drugs of abuse, such as cocaine, has recently been linked to alterations in adult neurogenesis in the hippocampus. The endogenous cannabinoid system modulates this proliferative response as demonstrated by the finding that pharmacological activation/blockade of cannabinoid CB1 and CB2 receptors not only modulates neurogenesis but also modulates cell death in the brain. In the present study, we evaluated whether the endogenous cannabinoid system affects cocaine-induced alterations in cell proliferation. To this end, we examined whether pharmacological blockade of either CB1 (Rimonabant, 3 mg/kg) or CB2 receptors (AM630, 3 mg/kg) would affect cell proliferation [the cells were labeled with 5-bromo-2'-deoxyuridine (BrdU)] in the subventricular zone (SVZ) of the lateral ventricle and the dentate subgranular zone (SGZ). Additionally, we measured cell apoptosis (as monitored by the expression of cleaved caspase-3) and glial activation [by analyzing the expression of glial fibrillary acidic protein (GFAP) and Iba-1] in the striatum and hippocampus during acute and repeated (4 days) cocaine administration (20 mg/kg). The results showed that acute cocaine exposure decreased the number of BrdU-immunoreactive (ir) cells in the SVZ and SGZ. In contrast, repeated cocaine exposure reduced the number of BrdU-ir cells only in the SVZ. Both acute and repeated cocaine exposure increased the number of cleaved caspase-3-, GFAP- and Iba1-ir cells in the hippocampus, and this effect was counteracted by AM630 or Rimonabant, which increased the number of BrdU-, GFAP-, and Iba1-ir cells in the hippocampus. These results indicate that the changes in neurogenic, apoptotic and gliotic processes that were produced by repeated cocaine administration were normalized by pharmacological blockade of CB1 and CB2. The restorative effects of cannabinoid receptor blockade on hippocampal cell proliferation were associated with the prevention of the induction of conditioned locomotion but not with the prevention of cocaine-induced sensitization.es
dc.description.versionYeses
dc.identifier.citationBlanco-Calvo E, Rivera P, Arrabal S, Vargas A, Pavón FJ, Serrano A, et al. Pharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat. Front Integr Neurosci. 2014; 7:106es
dc.identifier.doi10.3389/fnint.2013.00106
dc.identifier.essn1662-5145
dc.identifier.pmcPMC3884150
dc.identifier.pmid24409127
dc.identifier.urihttp://hdl.handle.net/10668/1613
dc.journal.titleFrontiers in integrative neuroscience
dc.language.isoen
dc.publisherFrontierses
dc.relation.publisherversionhttp://journal.frontiersin.org/Journal/10.3389/fnint.2013.00106/full#h1es
dc.rights.accessRightsopen access
dc.subjectCocainees
dc.subjectNeurogenesises
dc.subjectCannabinoid receptorses
dc.subjectRimonabantes
dc.subjectAM630es
dc.subjectInflammationes
dc.subjectHippocampuses
dc.subjectStriatumes
dc.subjectCocainaes
dc.subjectReceptor cannabinoide CB1es
dc.subjectReceptor cannabinoide CB2es
dc.subjectHipocampoes
dc.subjectNeostriadoes
dc.subjectRatases
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Heterocyclic Compounds::Alkaloids::Tropanes::Cocainees
dc.subject.meshMedical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesises
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, G-Protein-Coupled::Receptors, Cannabinoid::Receptor, Cannabinoid, CB1es
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, G-Protein-Coupled::Receptors, Cannabinoid::Receptor, Cannabinoid, CB2es
dc.subject.meshMedical Subject Headings::Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampuses
dc.subject.meshMedical Subject Headings::Anatomy::Nervous System::Central Nervous System::Brain::Prosencephalon::Telencephalon::Cerebrum::Basal Ganglia::Corpus Striatum::Neostriatumes
dc.subject.meshMedical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Ratses
dc.subject.meshMedical Subject Headings::Check Tags::Malees
dc.titlePharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat.es
dc.typeresearch article
dc.type.hasVersionVoR
dspace.entity.typePublication

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