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dc.contributor.authorPérez Martín, Margarita
dc.contributor.authorRivera, Patricia
dc.contributor.authorBlanco Calvo, Eduardo
dc.contributor.authorLorefice, Clara
dc.contributor.authorDecara, Juan
dc.contributor.authorPavón, Francisco Javier
dc.contributor.authorSerrano, Antonia
dc.contributor.authorRodríguez de Fonseca, Fernando
dc.contributor.authorSuárez, Juan
dc.date.accessioned2016-06-21T08:06:55Z
dc.date.available2016-06-21T08:06:55Z
dc.date.issued2016
dc.identifier.issn1662-4548
dc.identifier.urihttp://hdl.handle.net/10459.1/57238
dc.description.abstractPeroxisome proliferator-activated receptor alpha (PPARα) ligands have been shown to modulate recovery after brain insults such as ischemia and irradiation by enhancing neurogenesis. In the present study, we investigated the effect of the genetic deletion of PPARα receptors on the proliferative rate of neural precursor cells (NPC) in the adult brain. The study was performed in aged Pparα −/− mice exposed to nutritional (treats) and environmental (games) enrichments for 20 days. We performed immunohistochemical analyses of cells containing the replicating cell DNA marker 5-bromo-2′ -deoxyuridine (BrdU+) and the immature neuronal marker doublecortin (Dcx+) in the main neurogenic zones of the adult brain: subgranular zone of dentate gyrus (SGZ), subventricular zone of lateral ventricles (SVZ), and/or hypothalamus. Results indicated a reduction in the number of BrdU+ cells in the neurogenic zones analyzed as well as Dcx+ cells in the SGZ during aging (2, 6, and 18 months). Pparα deficiency alleviated the age-related reduction of NPC proliferation (BrdU+ cells) in the SVZ of the 18-months-old mice. While no genotype effect on NPC proliferation was detected in the SGZ during aging, an accentuated reduction in the number of Dcx+ cells was observed in the SGZ of the 6-months-old Pparα −/− mice. Exposing the 18-months-old mice to nutritional and environmental enrichments reversed the Pparα −/−-induced impairment of NPC proliferation in the neurogenic zones analyzed. The enriched environment did not modify the number of SGZ Dcx+ cells in the 18 months old Pparα −/− mice. These results identify PPARα receptors as a potential target to counteract the naturally observed decline in adult NPC proliferation associated with aging and impoverished environments.ca_ES
dc.description.sponsorshipGrant sponsor: 7th Framework Programme of European Union. Grant number: HEALTH-F2-2008-223713, REPROBESITY to FR. Grant sponsor: Instituto de Salud Carlos III (ISCIII), Ministerio de Economía y Competitividad (MINECO), UEERDF. Grant numbers: PI13/02261 to FR. and CP12/03109 to JS. Grant sponsor: Red de Trastornos Adictivos, ISCIII, MINECO. Grant number: RD12/0028/0001 to FR. Grant sponsor: Plan Nacional Sobre Drogas, Ministerio de Sanidad y Consumo. Grant number: PNSD2010/143 and PNSD2015/047 to JS. Grant sponsor: Fundació La Marató de TV3. Grant number: 386/C/2011. Grant sponsor: Consejería de Economía, Innovación y Ciencia, Junta de Andalucía, UE/ERDF. Grant numbers: PI45403 and CTS-8221 to FR. Grant sponsor: Consejería de Salud, Junta de Andalucía, UE/ERDF. Grant number: SAS111224 to FR. JS, FP and AS hold “Miguel Servet” research contracts from the National System of Health, ISCIII (grant numbers: CP12/03109, CP14/00212 and CP14/00173, respectively)ca_ES
dc.language.isoengca_ES
dc.publisherFrontiers Mediaca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.3389/fnins.2016.00089ca_ES
dc.relation.ispartofFrontiers in Neuroscience, 2016, vol. 10, núm. 89, p. 1-12ca_ES
dc.rightscc-by, (c) Pérez-Martín et al., 2016ca_ES
dc.subjectAgingca_ES
dc.subjectEnvironmentca_ES
dc.subjectPPARαca_ES
dc.subjectSubventricular zoneca_ES
dc.titleEnvironmental Enrichment, Age, and PPARα Interact to Regulate Proliferation in Neurogenic Nichesca_ES
dc.typearticleca_ES
dc.identifier.idgrec024947
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.3389/fnins.2016.00089
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/223713


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