Impaired locomotion and dopamine signaling in retinoid receptor mutant mice.
Fiche publication
Date publication
février 1998
Journal
Science (New York, N.Y.)
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre, Dr KASTNER Philippe, Dr GHYSELINCK Norbert, Dr KREZEL Wojciech
Tous les auteurs :
Krezel W, Ghyselinck N, Samad TA, Dupé V, Kastner P, Borrelli E, Chambon P
Lien Pubmed
Résumé
In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.
Mots clés
Animals, Cocaine, pharmacology, Corpus Striatum, metabolism, Dimerization, Dopamine, metabolism, Locomotion, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity, drug effects, Muscle, Skeletal, physiology, Parkinson Disease, etiology, Peripheral Nervous System, physiology, Receptors, Dopamine D1, genetics, Receptors, Dopamine D2, genetics, Receptors, Retinoic Acid, genetics, Retinoid X Receptors, Schizophrenia, etiology, Signal Transduction, Transcription Factors, genetics
Référence
Science. 1998 Feb;279(5352):863-7