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Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothalamus and striatum in a negative energy context.

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dc.contributor.authorRivera, Patricia
dc.contributor.authorBindila, Laura
dc.contributor.authorPastor, Antoni
dc.contributor.authorPérez-Martín, Margarita
dc.contributor.authorPavón, Francisco-Javier
dc.contributor.authorSerrano, Antonia
dc.contributor.authorde la Torre, Rafael
dc.contributor.authorLutz, Beat
dc.contributor.authorRodríguez de Fonseca, Fernando
dc.contributor.authorSuárez, Juan
dc.contributor.authoraffiliation[Rivera,P; Pavón,FJ; Serrano,A; Rodríguez de Fonseca,F; Suárez,J] UGC Salud Mental, Instituto de Investigación Biomédica (IBIMA), Universidad de Málaga-Hospital Universitario Regional de Málaga, Málaga, Spain. [Rivera,P; Pavón,FJ; Serrano,A; de la Torre,R; Rodríguez de Fonseca,F; Suárez,J] CIBER OBN, Instituto de Salud Carlos III, Madrid, Spain. [Bindila,L, Lutz,B] Institute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany. [Pastor,A; de la Torre,R] Institut Hospital del Mar d'Investigacions Mediques, Barcelona, Spain. [Pastor,A] Facultat de Medicina, Universitat Autonoma de Barcelona, Barcelona, Spain. [Pérez-Martín,M] Departamento de Biología Celular, Genética y Fisiología, Instituto de Investigación Biomédica (IBIMA), Universidad de Málaga, Málaga, Spain. [de la Torre, R] Facultat de Ciencies de la Salut i de la Vida, Universitat Pompeu Fabra (CEXS-UPF), Barcelona, Spain.
dc.date.accessioned2024-01-15T18:17:33Z
dc.date.available2024-01-15T18:17:33Z
dc.date.issued2015-03-27
dc.description.abstractEndocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamines oleoylethanolamide, palmitoylethanolamide and arachidonoylethanolamine, reduced the plasma levels of glucose, triglycerides and cholesterol, and induced a transitory body weight decrease. The hippocampi of repeated URB597-treated rats showed a reduced number of phospho-H3(+) and BrdU(+) subgranular cells as well as GFAP(+), Iba1(+) and cleaved caspase-3(+) cells, which was accompanied with decreased hippocampal expression of the cannabinoid CB1 receptor gene Cnr1 and Faah. In the hypothalami of these rats, the number of phospho-H3(+), GFAP(+) and 3-weeks-old BrdU(+) cells was specifically decreased. The reduced striatal expression of CB1 receptor in repeated URB597-treated rats was only associated with a reduced apoptosis. In contrast, the striatum of acute URB597-treated rats showed an increased number of subventricular proliferative, astroglial and apoptotic cells, which was accompanied with increased Faah expression. Main results indicated that FAAH inhibitor URB597 decreased neural proliferation, glia and apoptosis in a brain region-dependent manner, which were coupled to local changes in Faah and/or Cnr1 expression and a negative energy context.
dc.description.sponsorshipGrant sponsor: 7th Framework Programme of European Union; Grant number: HEALTH-F2-2008-223713, REPROBESITY to FR and BL; Grant sponsor: Ministerio de Ciencia e Innovación; Grant numbers: SAF2010-19087, SAF 2010-20521; Grant sponsor: Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, UE-ERDF; Grant number: CP12/03109; Grant sponsor: Red de Trastornos Adictivos; Grant numbers: RD12/0028/0001, RD12/0028/0009; Grant sponsor: CIBERobn; Grant sponsor: Plan Nacional Sobre Drogas, Ministerio de Sanidad y Consumo; Grant number: PNSD2010/143; Grant sponsor: Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, UE/ERDF; Grant numbers: CTS-433, P-11-CVI-07637; Grant sponsor: Consejería de Salud, Junta de Andalucía; Grant numbers: PI0232/2008, PI0029/2008, SAS111224; Grant sponsor: Fundació La Marató de TV3; Grant number: 386/C/2011; Grant sponsor: German Research Foundation DFG; Grant number: FOR629, project CP2 to BL. JS, FP, and AS hold “Miguel Servet” research contracts from the National System of Health, ISCIII (Grant numbers: CP12/03109, CP14/00212, CP14/00173 respectively).
dc.identifier.doi10.3389/fncel.2015.00098
dc.identifier.e-issn1662-5102es_ES
dc.identifier.journalFrontiers in Cellular Neurosciencees_ES
dc.identifier.otherhttp://hdl.handle.net/10668/2340
dc.identifier.pubmedID25870539es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17086
dc.language.isoeng
dc.publisherFrontiers Media
dc.relation.publisherversionhttp://journal.frontiersin.org/article/10.3389/fncel.2015.00098/fulles
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution 4.0 International*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subjectURB597
dc.subjectFAAH
dc.subjectCannabinoids
dc.subjectEnergy metabolism
dc.subjectNeurogenesis
dc.subjectGliosis
dc.subjectBromodesoxiuridina
dc.subjectCannabinoides
dc.subjectCarbamatos
dc.subjectCaspasa 3
dc.subjectMuerte celular
dc.subjectProliferación celular
dc.subjectColesterol
dc.subjectEndocannabinoides
dc.subjectEtanolaminas
dc.subjectGlucosa
dc.subjectHipocampo
dc.subjectHipotálamo
dc.subjectMicroglía
dc.subjectÁcidos oléicos
dc.subjectÁcidos palmíticos
dc.subjectRatas
dc.subjectReceptor cannabinoide CB1
dc.subjectTriglicéridos
dc.subjectAmidohidrolasas
dc.subjectApoptosis
dc.subjectAstrocitos
dc.subjectBenzamidas
dc.subjectPeso corporal
dc.subjectCerebro
dc.subject.meshAmidohydrolases
dc.subject.meshAnimals
dc.subject.meshApoptosis
dc.subject.meshAstrocytes
dc.subject.meshBenzamides
dc.subject.meshBody Weight
dc.subject.meshBrain
dc.subject.meshBromodeoxyuridine
dc.subject.meshCannabinoids
dc.subject.meshCarbamates
dc.subject.meshCaspases
dc.subject.meshCell Death
dc.subject.meshCell Proliferation
dc.subject.meshCholesterol
dc.subject.meshEndocannabinoids
dc.subject.meshEthanolamines
dc.subject.meshGliosis
dc.subject.meshGlucose
dc.subject.meshHippocampus
dc.subject.meshHypothalamus
dc.subject.meshMicroglia
dc.subject.meshNeurogenesis
dc.subject.meshOleic Acids
dc.subject.meshPalmitic Acids
dc.subject.meshRats
dc.subject.meshReceptor, Cannabinoid, CB1
dc.subject.meshTriglycerides
dc.titlePharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothalamus and striatum in a negative energy context.
dc.typeresearch article
dc.type.hasVersionVoR
dspace.entity.typePublication
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