Premium
Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine
Author(s) -
De Backer JeanFrançois,
Monlezun Stéphanie,
Detraux Bérangère,
Gazan Adeline,
Vanopdenbosch Laura,
Cheron Julian,
Cannazza Giuseppe,
Valverde Sébastien,
Cantacorps Lídia,
Nassar Mérie,
Venance Laurent,
Valverde Olga,
Faure Philippe,
Zoli Michele,
De Backer Olivier,
Gall David,
Schiffmann Serge N,
Kerchove d'Exaerde Alban
Publication year - 2018
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201745089
Subject(s) - humanities , library science , art , computer science
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 GABA ergic 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 ( NA c). This work identifies Maged1 as a critical molecule involved in cellular processes and behaviours related to addiction.