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

Autores
Blanco Calvo, Eduardo; Rivera, Patricia; Arrabal, Sergio; Vargas, Antonio; Pavon, Francisco Javier; Serrano, Antonia; Castilla Ortega, Estela; Galeano, Pablo; Rubio, Leticia; Suaréz, Juan; Rodríguez de Fonseca, Fernando
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Addiction 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 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 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.
Fil: Blanco Calvo, Eduardo. Universitat de Lleida; España
Fil: Rivera, Patricia. Universidad de Malaga; España
Fil: Arrabal, Sergio. Universidad de Malaga; España
Fil: Vargas, Antonio. Universidad de Malaga; España
Fil: Pavon, Francisco Javier. Universidad de Malaga; España
Fil: Serrano, Antonia. Universidad de Malaga; España
Fil: Castilla Ortega, Estela. Universidad de Malaga; España
Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Rubio, Leticia. Universidad de Malaga; España
Fil: Suaréz, Juan. Universidad de Malaga; España
Fil: Rodríguez de Fonseca, Fernando. Universidad de Malaga; España
Materia
Cocaina
Neurogenesis
Cannabinoid receptors
Rimonabant
AM630
Inflammation
Hippocampus
Striatum
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/7900
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/7900
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling 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 ratsBlanco Calvo, EduardoRivera, PatriciaArrabal, SergioVargas, AntonioPavon, Francisco JavierSerrano, AntoniaCastilla Ortega, EstelaGaleano, PabloRubio, LeticiaSuaréz, JuanRodríguez de Fonseca, FernandoCocainaNeurogenesisCannabinoid receptorsRimonabantAM630InflammationHippocampusStriatumhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Addiction 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 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 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.Fil: Blanco Calvo, Eduardo. Universitat de Lleida; EspañaFil: Rivera, Patricia. Universidad de Malaga; EspañaFil: Arrabal, Sergio. Universidad de Malaga; EspañaFil: Vargas, Antonio. Universidad de Malaga; EspañaFil: Pavon, Francisco Javier. Universidad de Malaga; EspañaFil: Serrano, Antonia. Universidad de Malaga; EspañaFil: Castilla Ortega, Estela. Universidad de Malaga; EspañaFil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Rubio, Leticia. Universidad de Malaga; EspañaFil: Suaréz, Juan. Universidad de Malaga; EspañaFil: Rodríguez de Fonseca, Fernando. Universidad de Malaga; EspañaFrontiers2014-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/7900Blanco Calvo, Eduardo; Rivera, Patricia; Arrabal, Sergio; Vargas, Antonio; Pavon, Francisco Javier; 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 rats; Frontiers; Frontiers in Integrative Neuroscience; 7; 106; 1-2014; 1-131662-5145enginfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884150/info:eu-repo/semantics/altIdentifier/url/http://journal.frontiersin.org/article/10.3389/fnint.2013.00106/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fnint.2013.00106info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:02:47Zoai:ri.conicet.gov.ar:11336/7900instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:02:47.701CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv 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 rats
title 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 rats
spellingShingle 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 rats
Blanco Calvo, Eduardo
Cocaina
Neurogenesis
Cannabinoid receptors
Rimonabant
AM630
Inflammation
Hippocampus
Striatum
title_short 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 rats
title_full 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 rats
title_fullStr 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 rats
title_full_unstemmed 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 rats
title_sort 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 rats
dc.creator.none.fl_str_mv Blanco Calvo, Eduardo
Rivera, Patricia
Arrabal, Sergio
Vargas, Antonio
Pavon, Francisco Javier
Serrano, Antonia
Castilla Ortega, Estela
Galeano, Pablo
Rubio, Leticia
Suaréz, Juan
Rodríguez de Fonseca, Fernando
author Blanco Calvo, Eduardo
author_facet Blanco Calvo, Eduardo
Rivera, Patricia
Arrabal, Sergio
Vargas, Antonio
Pavon, Francisco Javier
Serrano, Antonia
Castilla Ortega, Estela
Galeano, Pablo
Rubio, Leticia
Suaréz, Juan
Rodríguez de Fonseca, Fernando
author_role author
author2 Rivera, Patricia
Arrabal, Sergio
Vargas, Antonio
Pavon, Francisco Javier
Serrano, Antonia
Castilla Ortega, Estela
Galeano, Pablo
Rubio, Leticia
Suaréz, Juan
Rodríguez de Fonseca, Fernando
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Cocaina
Neurogenesis
Cannabinoid receptors
Rimonabant
AM630
Inflammation
Hippocampus
Striatum
topic Cocaina
Neurogenesis
Cannabinoid receptors
Rimonabant
AM630
Inflammation
Hippocampus
Striatum
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Addiction 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 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 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.
Fil: Blanco Calvo, Eduardo. Universitat de Lleida; España
Fil: Rivera, Patricia. Universidad de Malaga; España
Fil: Arrabal, Sergio. Universidad de Malaga; España
Fil: Vargas, Antonio. Universidad de Malaga; España
Fil: Pavon, Francisco Javier. Universidad de Malaga; España
Fil: Serrano, Antonia. Universidad de Malaga; España
Fil: Castilla Ortega, Estela. Universidad de Malaga; España
Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Rubio, Leticia. Universidad de Malaga; España
Fil: Suaréz, Juan. Universidad de Malaga; España
Fil: Rodríguez de Fonseca, Fernando. Universidad de Malaga; España
description Addiction 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 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 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.
publishDate 2014
dc.date.none.fl_str_mv 2014-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/7900
Blanco Calvo, Eduardo; Rivera, Patricia; Arrabal, Sergio; Vargas, Antonio; Pavon, Francisco Javier; 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 rats; Frontiers; Frontiers in Integrative Neuroscience; 7; 106; 1-2014; 1-13
1662-5145
url http://hdl.handle.net/11336/7900
identifier_str_mv Blanco Calvo, Eduardo; Rivera, Patricia; Arrabal, Sergio; Vargas, Antonio; Pavon, Francisco Javier; 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 rats; Frontiers; Frontiers in Integrative Neuroscience; 7; 106; 1-2014; 1-13
1662-5145
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884150/
info:eu-repo/semantics/altIdentifier/url/http://journal.frontiersin.org/article/10.3389/fnint.2013.00106/full
info:eu-repo/semantics/altIdentifier/doi/10.3389/fnint.2013.00106
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers
publisher.none.fl_str_mv Frontiers
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.982451

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