Journal article
bioRxiv, 2019
APA
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Borie, A., Dromard, Y., Dufner, D., Pollozi, E., Huzard, D., Tömböli, C., … Jeanneteau, F. (2019). Control of Social Withdrawal of Mice Deficient for the Autism Gene Magel2 by Restoration of Vasopressin-Oxytocin Dialogue in Septum. BioRxiv.
Chicago/Turabian
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Borie, A., Y. Dromard, Djodi Dufner, E. Pollozi, Damien Huzard, Csaba Tömböli, A. Olma, et al. “Control of Social Withdrawal of Mice Deficient for the Autism Gene Magel2 by Restoration of Vasopressin-Oxytocin Dialogue in Septum.” bioRxiv (2019).
MLA
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Borie, A., et al. “Control of Social Withdrawal of Mice Deficient for the Autism Gene Magel2 by Restoration of Vasopressin-Oxytocin Dialogue in Septum.” BioRxiv, 2019.
BibTeX Click to copy
@article{a2019a,
title = {Control of Social Withdrawal of Mice Deficient for the Autism Gene Magel2 by Restoration of Vasopressin-Oxytocin Dialogue in Septum},
year = {2019},
journal = {bioRxiv},
author = {Borie, A. and Dromard, Y. and Dufner, Djodi and Pollozi, E. and Huzard, Damien and Tömböli, Csaba and Olma, A. and Manning, M. and Colson, P. and Guillon, G. and Muscatelli, F. and Desarménien, M. and Jeanneteau, F.}
}
In brief Collective actions of vasopressin and oxytocin determine social salience. Borie et al. find that the degree of social novelty moderates a dialogue between networks secreting social salience hormones in the lateral septum, a region organizing sequential content of sensory experiences. Social withdrawal of mice lacking the autism gene Magel2 is alleviated by restoration of dialogue-lead with vasopressin. Highlights Social novelty activates the hypothalamoseptal vasopressin (AVP) pathway Social habituation activates the hypothalamoseptal oxytocin (OXT) pathway Disarray of AVP and OXT responses in LS mimics social disabilities of Magel2 KO mice Paucity of cells detecting coincident AVP and OXT in LS of Magel2 KO mice Sociability restored in Magel2 KO mice by AVP-priming of OXT responses in LS 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.