Journal
EMBO REPORTS
Volume 19, Issue 9, Pages -Publisher
WILEY
DOI: 10.15252/embr.201745089
Keywords
amygdala; dopamine; drug sensitization; nucleus accumbens; prefrontal cortex
Categories
Funding
- FRS-FNRS
- Van Buuren Funds
- Fonds Erasme
- FRIA (Belgium)
- Walloon Region
- FMRE-Belgium
- FRS-FNRS (Belgium)
- Interuniversity Attraction Pole from Belgian Federal Scientific Affairs [IUAP-P7/10]
- Centre National de la Recherche Scientifique CNRS [UMR 8246]
- University Pierre et Marie Curie [UM 119]
- Institut national de la sante et de la recherche medicale INSERM [U1130]
- Spanish Ministry of Economy [SAF2016-75966R-FEDER]
- Generalitat de Catalunya [2014SGR34]
- UE Medbioinformatic Project [634143]
- LabEx Paris-Sciences et Lettres (PSL)
- Italian Ministry of Health [RF2009-1549619]
- Action de Recherche Concertee (FWB)
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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.
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