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An Early Postnatal Oxytocin Treatment Prevents Social and Learning Deficits in Adult Mice Deficient for Magel2, a Gene Involved in Prader-Willi Syndrome and Autism.
Hamid Meziane
1 ,
Fabienne Schaller
2 ,
Sylvian Bauer
2 ,
Claude Villard
3 ,
Valery Matarazzo
2 ,
Fabrice Riet
1 ,
Gilles Guillon
4 ,
Daniel Lafitte
3 ,
Michel G Desarmenien
4 ,
Maithé Tauber
5 ,
Françoise Muscatelli
6
Jul 15 2015
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Abstract
Mutations of MAGEL2 have been reported in patients presenting with autism, and loss of MAGEL2 is also associated with Prader-Willi syndrome, a neurodevelopmental genetic disorder. This study aimed to determine the behavioral phenotype of Magel2-deficient adult mice, to characterize the central oxytocin (OT) system of these mutant mice, and to test the curative effect of a peripheral OT treatment just after birth.