Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine

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dc.contributor.author	De Backer, Jean-François
dc.contributor.author	Monlezun, Stéphanie
dc.contributor.author	Detraux, Bérangère
dc.contributor.author	Gazan, Adeline
dc.contributor.author	Vanopdenbosch, Laura
dc.contributor.author	Cheron, Julian
dc.contributor.author	Cannazza, Giuseppe
dc.contributor.author	Valverde, Sébastien
dc.contributor.author	Cantacorps, Lídia
dc.contributor.author	Nassar, Mérie
dc.contributor.author	Venance, Laurent
dc.contributor.author	Valverde Granados, Olga
dc.contributor.author	Faure, Philippe
dc.contributor.author	Zoli, Michele
dc.contributor.author	De Backer, Olivier
dc.contributor.author	Gall, David
dc.contributor.author	Schiffmann, Serge N.
dc.contributor.author	de Kerchove d'Exaerde, Alban
dc.date	2018
dc.identifier.citation	De Backer JF, Monlezun S, Detraux B, Gazan A, Vanopdenbosch L, Cheron J, Cannazza G, Valverde S, Cantacorps L, Nassar M, Venance L, Valverde O, Faure P, Zoli M, De Backer O, Gall D, Schiffmann SN, de Kerchove d'Exaerde A. Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine. EMBO Rep. 2018; 19(9):e45089. DOI: 10.15252/embr.201745089
dc.identifier.citation	1469-221X
dc.identifier.citation	http://dx.doi.org/10.15252/embr.201745089
dc.identifier.uri	http://hdl.handle.net/10230/37044
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Wiley-Blackwell
dc.relation	info:eu-repo/grantAgreement/EC/H2020/634143
dc.relation	info:eu-repo/grantAgreement/ES/1PE/SAF2016-75966R
dc.rights	info:eu-repo/semantics/openAccess
dc.rights	This is the pre-peer reviewed version of the following article: De Backer JF, Monlezun S, Detraux B, Gazan A, Vanopdenbosch L, Cheron J, Cannazza G, Valverde S, Cantacorps L, Nassar M, Venance L, Valverde O, Faure P, Zoli M, De Backer O, Gall D, Schiffmann SN, de Kerchove d'Exaerde A. Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine. EMBO Rep. 2018; 19(9):e45089. DOI 10.15252/embr.201745089, which has been published in final form at http://dx.doi.org10.15252/embr.201745089. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
dc.subject	Amygdala
dc.subject	Dopamine
dc.subject	Drug sensitization
dc.subject	Nucleus accumbens
dc.subject	Prefrontal cortex
dc.title	Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/acceptedVersion
dc.description.abstract	Melanoma antigen genes (Mage) were first described as tumour markers. However, some of Mage are also expressed in healthy cells where their functions remain poorly understood. Here, we describe an unexpected role for one of these genes, Maged1, in the control of behaviours related to drug addiction. Mice lacking Maged1 are insensitive to the behavioural effects of cocaine as assessed by locomotor sensitization, conditioned place preference (CPP) and drug self-administration. Electrophysiological experiments in brain slices and conditional knockout mice demonstrate that Maged1 is critical for cortico-accumbal neurotransmission. Further, expression of Maged1 in the prefrontal cortex (PFC) and the amygdala, but not in dopaminergic or striatal and other GABAergic neurons, is necessary for cocaine-mediated behavioural sensitization, and its expression in the PFC is also required for cocaine-induced extracellular dopamine (DA) release in the nucleus accumbens (NAc). This work identifies Maged1 as a critical molecule involved in cellular processes and behaviours related to addiction.
dc.description.abstract	JFDB was supported by the Aspirant PhD fellowship from the FRS-FNRS and Van Buuren Funds, BD and AG are supported by the Aspirant PhD fellowship from the FRSFNRS, JC was supported by a fellowship from the Fonds Erasme and SM was supported by a PhD fellowship from FRIA (Belgium) and a Biowin Program from the Walloon Region. AKE is a Research Director of the FRS-FNRS and an investigator of WELBIO. This study was supported by FMRE-Belgium, FRSFNRS (Belgium), Interuniversity Attraction Pole (IUAP-P7/10) from Belgian Federal Scientific Affairs and Action de Recherche Concertée (FWB). The Foundation for Medical Research (FRM, Equipe FRM 2013 to PF), the Centre National de la Recherche Scientifique CNRS UMR 8246, the University Pierre et Marie Curie UM 119, Institut national de la santé et de la recherche médicale INSERM U1130. The Spanish Ministry of Economy (SAF2016-75966R-FEDER), the Generalitat de Catalunya (2014SGR34) and UE Medbioinformatic Project (grant number 634143) to OV. MN was supported by the LabEx Paris-Sciences et Lettres (PSL). The Italian Ministry of Health (RF2009-1549619) to MZ. The Fonds de la Recherche Scientifique-FNRS of the Fédération Wallonie-Bruxelles to ODB.

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