Please use this identifier to cite or link to this item: http://hdl.handle.net/10668/2227
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dc.contributor.authorBlanco, Eduardo-
dc.contributor.authorPavón, Francisco J-
dc.contributor.authorPalomino, Ana-
dc.contributor.authorLuque-Rojas, María Jesús-
dc.contributor.authorSerrano, Antonia-
dc.contributor.authorRivera, Patricia-
dc.contributor.authorBilbao, Ainhoa-
dc.contributor.authorAlen, Francisco-
dc.contributor.authorVida, Margarita-
dc.contributor.authorSuárez, Juan-
dc.contributor.authorRodríguez de Fonseca, Fernando-
dc.date.accessioned2016-06-28T07:26:00Z-
dc.date.available2016-06-28T07:26:00Z-
dc.date.issued2015-01-31-
dc.identifier.citationBlanco E, Pavon FJ, Palomino A, Luque-Rojas MJ, Serrano A, Rivera P, et al. Cocaine-induced behavioral sensitization is associated with changes in the expression of endocannabinoid and glutamatergic signaling systems in the mouse prefrontal cortex. Int J Neuropsychopharmacol. 2014;18(1). pii: pyu024.es
dc.identifier.issn1469-5111 (Online)-
dc.identifier.issn1461-1457 (Print)-
dc.identifier.otherPMC4368868-
dc.identifier.urihttp://hdl.handle.net/10668/2227-
dc.descriptionJournal Article; Research Support, Non-U.S. Gov't;es
dc.description.abstractBACKGROUND Endocannabinoids modulate the glutamatergic excitatory transmission by acting as retrograde messengers. A growing body of studies has reported that both signaling systems in the mesocorticolimbic neural circuitry are involved in the neurobiological mechanisms underlying drug addiction. METHODS We investigated whether the expression of both endocannabinoid and glutamatergic systems in the prefrontal cortex (PFC) were altered by an acute and/or repeated cocaine administration schedule that resulted in behavioral sensitization. We measured the protein and mRNA expression of the main endocannabinoid metabolic enzymes and the cannabinoid receptor type 1 (CB1). We also analyzed the mRNA expression of relevant components of the glutamate-signaling system, including glutamate-synthesizing enzymes, metabotropic receptors, and ionotropic receptors. RESULTS Although acute cocaine (10 mg/kg) produced no significant changes in the endocannabinoid-related proteins, repeated cocaine administration (20 mg/kg daily) induced a pronounced increase in the CB1 receptor expression. In addition, acute cocaine administration (10 mg/kg) in cocaine-sensitized mice (referred to as cocaine priming) induced a selective increase in the endocannabinoid-degrading enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). These protein changes were accompanied by an overall decrease in the ratios of endocannabinoid synthesis/degradation, especially the N-acyl phosphatidylethanolamine phospholipase D/FAAH and diacylglycerol lipase alpha/MAGL ratios. Regarding mRNA expression, while acute cocaine administration produced a decrease in CB1 receptors and N-acyl phosphatidylethanolamine phospholipase D, repeated cocaine treatment enhanced CB1 receptor expression. Cocaine-sensitized mice that were administered priming injections of cocaine mainly displayed an increased FAAH expression. These endocannabinoid changes were associated with modifications in glutamatergic transmission-related genes. An overall decrease was observed in the mRNA expression of the glutamate-synthesizing gene kidney-type glutaminase (KGA), the metabotropic glutamate receptors (mGluR3 and GluR), and subunits of NMDA ionotropic receptors (NR1, NR2A, NR2B and NR2C) after acute cocaine administration, while mice repeatedly exposed to cocaine only displayed an increase in NR2C. However, in cocaine-sensitized mice primed with cocaine, this inhibition was reversed and a strong increase was detected in the mGluR5, NR2 subunits, and both GluR1 and GluR3. CONCLUSIONS These findings indicate that cocaine sensitization is associated with an endocannabinoid downregulation and a hyperglutamatergic state in the PFC that, overall, contribute to an enhanced glutamatergic input into PFC-projecting areas.es
dc.description.sponsorshipThis work was supported by Ministerio de Ciencia e Innovación (PI13/02261 and SAF 2010–20521), Instituto de Salud Carlos III (ISCIII), Ministerio de Economía y Competitividad, Red de Trastornos Adictivos (RD12/0028/0001), Plan Nacional Sobre Drogas, Ministerio de Sanidad y Consumo (PNSD2013/049), Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, UE/ERDF (CTS-433 and P-11-CVI-07637), Consejería de Salud, and Junta de Andalucía (PI0232/2008, PI0029/2008 and SAS111224).es
dc.language.isoenes
dc.publisherOxford University Presses
dc.relation.ispartofThe International Journal of Neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP)es
dc.subjectCannabinoides
dc.subjectCocainees
dc.subjectSensitizationes
dc.subjectGlutamatees
dc.subjectPrefrontal cortexes
dc.subjectCocaínaes
dc.subjectInhibidores de la captación de dopaminaes
dc.subjectDiscinesia inducida por medicamentoses
dc.subjectCorteza prefrontales
dc.subjectARN mensajeroes
dc.subjectReceptor cannabinoide CB1es
dc.subjectReceptores de glutamatoes
dc.subjectDopamine Uptake Inhibitorses
dc.subject.meshMedical Subject Headings::Organisms::Eukaryota::Animalses
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Organic Chemicals::Aza Compounds::Azabicyclo Compounds::Tropanes::Cocainees
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Neurotransmitter Uptake Inhibitors::Dopamine Uptake Inhibitorses
dc.subject.meshMedical Subject Headings::Diseases::Substance-Related Disorders::Poisoning::Drug Toxicity::Dyskinesia, Drug-Inducedes
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoidses
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Amino Acids::Amino Acids, Acidic::Glutamic Acides
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases::Glutaminasees
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Esterases::Carboxylic Ester Hydrolases::Lipoprotein Lipasees
dc.subject.meshMedical Subject Headings::Check Tags::Malees
dc.subject.meshMedical Subject Headings::Organisms::Eukaryota::Animals::Animal Population Groups::Animals, Laboratory::Animals, Inbred Strains::Mice, Inbred Strains::Mice, Inbred C57BLes
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Esterases::Carboxylic Ester Hydrolases::Monoacylglycerol Lipaseses
dc.subject.meshMedical Subject Headings::Anatomy::Nervous System::Central Nervous System::Brain::Prosencephalon::Telencephalon::Cerebrum::Cerebral Cortex::Frontal Lobe::Prefrontal Cortexes
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Nucleic Acids, Nucleotides, and Nucleosides::Nucleic Acids::RNA::RNA, Messengeres
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, Neurotransmitter::Receptors, Amino Acid::Receptors, Glutamatees
dc.subject.meshMedical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolaseses
dc.titleCocaine-induced behavioral sensitization is associated with changes in the expression of endocannabinoid and glutamatergic signaling systems in the mouse prefrontal cortex.es
dc.typeinfo:eu-repo/semantics/articlees
dc.description.versionYeses
dc.identifier.pmid25539508-
dc.rights.accessRightsAcceso abiertoes
dc.identifier.doi10.1093/ijnp/pyu024-
dc.type.versioninfo:eu-repo/semantics/publishedes
dc.relation.publisherversionhttp://ijnp.oxfordjournals.org/content/18/1/pyu024.longes
dc.contributor.authoraffiliation[Blanco,E; Pavón,FJ; Palomino,A; Luque-Rojas,MJ; Serrano,A; Rivera,P; Alen,F; Vida,M; Suárez,J; Rodríguez de Fonseca,F] Unidad de Gestión Clínica de Salud Mental, Instituto IBIMA-Hospital Regional Universitario de Málaga, Málaga, Spain. [Blanco,E] Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Facultad de Psicología, Universidad de Málaga, Málaga, Spain. [Bilbao,A] Institute of Psychopharmacology, Central Institute of Mental Health, Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.es
dc.type.subtypeArtículoes
Appears in Collections:01- Artículos - Hospital Regional de Málaga
01- Artículos - IBIMA. Instituto de Investigación Biomédica de Málaga

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