Disrupting D1-NMDA or D2-NMDA receptor heteromerization prevents cocaine's rewarding effects but preserves natural reward processing.
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ABSTRACT:
SUBMITTER: Andrianarivelo A
PROVIDER: S-EPMC8528421 | biostudies-literature | 2021 Oct
REPOSITORIES: biostudies-literature
Publications
Disrupting D1-NMDA or D2-NMDA receptor heteromerization prevents cocaine's rewarding effects but preserves natural reward processing.
Andrianarivelo Andry A Saint-Jour Estefani E Pousinha Paula P Fernandez Sebastian P SP Petitbon Anna A De Smedt-Peyrusse Veronique V Heck Nicolas N Ortiz Vanesa V Allichon Marie-Charlotte MC Kappès Vincent V Betuing Sandrine S Walle Roman R Zhu Ying Y Joséphine Charlène C Bemelmans Alexis-Pierre AP Turecki Gustavo G Mechawar Naguib N Javitch Jonathan A JA Caboche Jocelyne J Trifilieff Pierre P Barik Jacques J Vanhoutte Peter P
Science advances 20211020 43
Addictive drugs increase dopamine in the nucleus accumbens (NAc), where it persistently shapes excitatory glutamate transmission and hijacks natural reward processing. Here, we provide evidence, from mice to humans, that an underlying mechanism relies on drug-evoked heteromerization of glutamate <i>N</i>-methyl-d-aspartate receptors (NMDAR) with dopamine receptor 1 (D1R) or 2 (D2R). Using temporally controlled inhibition of D1R-NMDAR heteromerization, we unraveled their selective implication in ...[more]
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