Sexually dimorphic oxytocin circuits drive intragroup social conflict and aggression in wild house mice.

Autor: Sofer Y; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel., Zilkha N; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel., Gimpel E; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel., Wagner S; Sagol Department of Neurobiology, the Integrated Brain and Behavior Research Center, University of Haifa, Haifa, Israel., Chuartzman SG; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel., Kimchi T; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel. tali.kimchi@weizmann.ac.il.
Jazyk: angličtina
Zdroj: Nature neuroscience [Nat Neurosci] 2024 Aug; Vol. 27 (8), pp. 1565-1573. Date of Electronic Publication: 2024 Jul 05.
DOI: 10.1038/s41593-024-01685-5
Abstrakt: In nature, both males and females engage in competitive aggressive interactions to resolve social conflicts, yet the behavioral principles guiding such interactions and their underlying neural mechanisms remain poorly understood. Through circuit manipulations in wild mice, we unveil oxytocin-expressing (OT + ) neurons in the hypothalamic paraventricular nucleus (PVN) as a neural hub governing behavior in dyadic and intragroup social conflicts, influencing the degree of behavioral sexual dimorphism. We demonstrate that OT + PVN neurons are essential and sufficient in promoting aggression and dominance hierarchies, predominantly in females. Furthermore, pharmacogenetic activation of these neurons induces a change in the 'personality' traits of the mice within groups, in a sex-dependent manner. Finally, we identify an innervation from these OT neurons to the ventral tegmental area that drives dyadic aggression, in a sex-specific manner. Our data suggest that competitive aggression in naturalistic settings is mediated by a sexually dimorphic OT network connected with reward-related circuitry.
(© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.)
Databáze: MEDLINE
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