Working memory deficits in retinoid X receptor gamma-deficient mice.
Fiche publication
Date publication
mai 2005
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre, Dr KREZEL Wojciech
Tous les auteurs :
Wietrzych M, Meziane H, Sutter A, Ghyselinck N, Chapman PF, Chambon P, Krezel W
Lien Pubmed
Résumé
Retinoid signaling has been recently shown to be required for mnemonic functions in rodents. To dissect the behavioral and molecular mechanisms involved in this requirement, we have analyzed the spatial and recognition working memory in mice carrying null mutations of retinoid receptors RARbeta and RXRgamma. Double mutants appeared deficient in spatial working memory as tested in spontaneous alternation in the Y-maze and delayed nonmatch to place (DNMTP) test in the T-maze. These mutant mice did acquire, however, spatial place reference or right/left discrimination tasks in the T-maze set-up, indicating that basic sensorimotor functions, spatial orientation, and motivational factors are unlikely to account for deficits in working memory-sensitive tasks. Double-mutant mice were also deficient in novel object recognition at intermediate, but not short delays. RXRgamma appeared to be the functionally predominant receptor in modulation of the working memory, as RXRgamma, but not RARbeta single null mutant mice exhibited deficits similar to those observed in the double mutants. The mechanism of this modulation is potentially related to functions of RXRgamma in frontal and perirhinal cortex, structures in which we detected RXRgamma expression and which are functionally implicated in working memory processes.
Référence
Learn Mem. 2005 May-Jun;12(3):318-26