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Glucocorticoids regulation of FosB/ΔFosB expression induced by chronic opiate exposure in the brain stress system

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dc.contributor.authorGarcía Pérez, Daniel
dc.contributor.authorNúñez Parra, Cristina
dc.contributor.authorLaorden Carrasco, María Luisa
dc.contributor.authorMilanés Maquilón, María Victoria
dc.contributor.departmentFarmacología
dc.contributor.otherFacultades de la UMU::Facultad de Medicina
dc.date.accessioned2026-02-12T18:47:29Z
dc.date.available2026-02-12T18:47:29Z
dc.date.copyright© 2012 García-Pérez et al.
dc.date.issued2012-11-21
dc.description.abstractChronic use of drugs of abuse profoundly alters stress-responsive system. Repeated exposure to morphine leads to accumulation of the transcription factor ΔFosB, particularly in brain areas associated with reward and stress. The persistent effects of ΔFosB on target genes may play an important role in the plasticity induced by drugs of abuse. Recent evidence suggests that stress-related hormones (e.g., glucocorticoids, GC) may induce adaptations in the brain stress system that is likely to involve alteration in gene expression and transcription factors. This study examined the role of GC in regulation of FosB/ΔFosB in both hypothalamic and extrahypothalamic brain stress systems during morphine dependence. For that, expression of FosB/ΔFosB was measured in control (sham-operated) and adrenalectomized (ADX) rats that were made opiate dependent after ten days of morphine treatment. In sham-operated rats, FosB/ΔFosB was induced after chronic morphine administration in all the brain stress areas investigated: nucleus accumbens(shell) (NAc), bed nucleus of the stria terminalis (BNST), central amygdala (CeA), hypothalamic paraventricular nucleus (PVN) and nucleus of the solitary tract noradrenergic cell group (NTS-A2). Adrenalectomy attenuated the increased production of FosB/ΔFosB observed after chronic morphine exposure in NAc, CeA, and NTS. Furthermore, ADX decreased expression of FosB/ΔFosB within CRH-positive neurons of the BNST, PVN and CeA. Similar results were obtained in NTS-A2 TH-positive neurons and NAc pro-dynorphin-positive neurons. These data suggest that neuroadaptation (estimated as accumulation of FosB/ΔFosB) to opiates in brain areas associated with stress is modulated by GC, supporting the evidence of a link between brain stress hormones and addiction.
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dc.identifier.citationPLoS ONE, 2012, Vol. 7 (11): e50264
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0050264
dc.identifier.eissn1932-6203
dc.identifier.urihttp://hdl.handle.net/10201/204621
dc.languageeng
dc.publisherPublic Library of Science
dc.relationThis work was supported by the following grants: Ministerio de Ciencia e Imnovación (SAF/FEDER 2009-07178 and SAF/FEDER 2010-17907), Spain; Red de Trastornos Adictivos (RD06/0001/1006 and RD06/0001/1001), Spain; Fundación Séneca, Agencia Regional de Ciencia y Tecnología Región de Murcia (15405/PI10), Spain. DG-P is supported by a fellowship from the Ministerio de Ciencia e Innovación (AP2009-2379).
dc.relation.publisherversionhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050264
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleGlucocorticoids regulation of FosB/ΔFosB expression induced by chronic opiate exposure in the brain stress system
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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