Control of Social Withdrawal of Mice Deficient for the Autism Gene Magel2 by Restoration of Vasopressin-Oxytocin Dialogue in Septum

Amélie M. Borie, Yann Dromard, Djodi Dufner, Emi Pollozi, Damien Huzard, Csaba Tömböli, Aleksandra Olma, Maurice Manning, Pascal Colson, Gilles Guillon, Françoise Muscatelli, Michel G. Desarménien, Freddy Jeanneteau
2019 · doi:10.1101/800425
preprint OA: closed
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Abstract

Summary Intellectual and social disabilities are common comorbidities in adolescents and adults with Magel2 gene deficiency characterizing the Prader-Willi and Schaaf-Yang neurodevelopmental syndromes. The cellular and molecular mechanisms underlying the risk for autism in these syndromes are unexplored. Here we used Magel2 knockout mice combined with optogenetic/pharmacological tools to characterize disease modifications in the social brain network. We find that the degree of social novelty moderates a dialogue between vasopressin and oxytocin in the lateral septum, a region organizing sequential content of sensory experiences. Social withdrawal of mice lacking Magel2 is alleviated by restoration of dialogue-lead by vasopressin. This preclinical study identifies the collective actions of vasopressin and oxytocin in the lateral septum as a key factor in the pathophysiology.

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