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Regulation of glial markers expression in the rat basolateral amygdala and hippocampus during morphine aversive memory retrieval and its extinction

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dc.contributor.authorFranco García, Aureliio
dc.contributor.authorGómez Murcia, Victoria
dc.contributor.authorNúñez Parra, Cristina
dc.contributor.departmentFarmacología
dc.date.accessioned2026-04-15T08:46:26Z
dc.date.available2026-04-15T08:46:26Z
dc.date.copyright© The Author(s) 2025
dc.date.issued2025-12-15
dc.description.abstractBackground Opioid use disorder is driven by neurobehavioral adaptations where environmental cues trigger relapse. Consequently, extinction therapy (ET) aims to modify drug-associated memories but has limited long-term efficacy. Recently, evidence suggested that glial cells may contribute to neuroplasticity phenomena in addiction. In this sense, this study examined whether aversive memories of morphine withdrawal and their extinction induce transcriptional changes in glial markers (gfap, aif1, itgam, klf4) in key memory-related regions: the basolateral amygdala (BLA) and hippocampus (dentate gyrus [DG] and CA1). Results Using the conditioned place aversion (CPA) paradigm in rats, we assessed avoidance behavior after naloxone-precipitated withdrawal and its extinction. Transcriptional analyses did not reveal major changes in the BLA. However, in CA1, downregulation of microglial markers cooccurred with aversive memory retrieval and restored after extinction. Moreover, one of the microglial markers, klf4, was reduced concomitantly with extinction memory retrieval in the DG. Correlation analyses showed negative associations between microglial markers and aversive memory strength, suggesting glial involvement in withdrawal-related learning. Conclusions These findings might indicate that microglial activity in CA1 plays a role in opioid withdrawal-associated memories, and extinction training might be returning these effects to basal levels. Therefore, targeting glial responses could provide new therapeutic strategies to prevent relapse.
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dc.format.extent14
dc.identifier.citationFranco-García et al. Behavioral and Brain Functions (2026) 22:4
dc.identifier.doi10.1186/s12993-025-00313-x
dc.identifier.urihttp://hdl.handle.net/10201/225681
dc.languageeng
dc.relationAgencia Estatal de Investigación. MCIN/AEI/10.13039/501100011033, ERDF A way of making Europe (SAF2017-85679-R y PID2020-113557RB-I00), through the regional call Fundación Séneca, Agencia de Ciencia y Tecnología de la Región de Murcia. Ayudas a proyectos para el desarrollo de investigación científica y técnica por grupos competitivos, Programa Regional de Fomento de la Investigación Científica y Técnica de Excelencia (Plan de Actuación 2022; 21133/SF/19; 21905/PI/22). Ministerio de Universidades. Programa Ayuda para la Formación de Profesorado Universitario (FPU19/01722).
dc.relation.publisherversionhttps://link.springer.com/article/10.1186/s12993-025-00313-x
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectWithdrawal, CPA
dc.subjectCPA
dc.subjectGlia
dc.subjectMemory
dc.subjectAmygdala
dc.subjectHippocampus
dc.subjectMorphine
dc.subject.odsObjetivo 3: Salud
dc.titleRegulation of glial markers expression in the rat basolateral amygdala and hippocampus during morphine aversive memory retrieval and its extinction
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublicationes
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relation.isAuthorOfPublication353c85df-d611-4999-b8b7-960dd35d1011
relation.isAuthorOfPublication.latestForDiscoveryc687f206-85db-4d6a-9b02-9ded2f03e259
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