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Maternal hormones engage a dormant monomorphic aggression circuit, leading to the introduction of an innate behavior in adulthood in females

Stagkourakis, Stefanos and Williams, Paul and Spigolon, Giada and Khanal, Shreya and Ziegler, Katharina and Heikkinen, Laura and Fisone, Gilberto and Broberger, Christian (2023) Maternal hormones engage a dormant monomorphic aggression circuit, leading to the introduction of an innate behavior in adulthood in females. . (Unpublished)

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Aggression - a sexually dimorphic behavior, is prevalent in males and typically absent in virgin females. Following parturition, however, the transient expression of aggression in adult females ensures the pups’ defense from predators and infanticide. While maternal hormones are known to elicit nursing, whether they play a role in the expression of maternal aggression remains unknown. Here we show that a molecularly defined subset of ventral premammillary (PMvᴰᴬᵀ) neurons, instrumental for intermale aggression, switch into a hyperexcitable state during lactation. We identify that the maternal hormones prolactin and oxytocin excite these cells, an effect mediated through T-type Ca²⁺ channels. Optogenetic manipulation or genetic ablation of PMvᴰᴬᵀ neurons profoundly affects maternal aggression, while activation of these neurons impairs the expression of non-aggression-related behaviors. This work identifies a monomorphic neural substrate that incorporates hormonal cues to enable the transient expression of a dormant behavioral program in adult females.

Item Type:Report or Paper (Discussion Paper)
Related URLs:
URLURL TypeDescription Paper
Stagkourakis, Stefanos0000-0003-1218-791X
Williams, Paul0000-0001-7779-3107
Spigolon, Giada0000-0002-1704-8372
Khanal, Shreya0000-0002-7403-5631
Ziegler, Katharina0000-0003-2111-8916
Heikkinen, Laura0000-0002-3683-6120
Fisone, Gilberto0000-0002-0719-8000
Broberger, Christian0000-0002-7050-8809
Additional Information:The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license. Members of the Broberger laboratory are thanked for discussion during the preparation of this manuscript. This study was made possible by a European Research Council starting grant (ENDOSWITCH 261286), the Swedish Research Council (2018-02480), the Strategic Research Program in Diabetes at Karolinska Institutet, Hjärnfonden (the Swedish Brain Foundation), Novo Nordisk Fonden, Wenner-Gren Foundation funding, and internal funds from Karolinska Institutet. Author contributions. S.S. and C.B. conceived the study and wrote the manuscript. S.S. designed, performed, and analyzed experiments. P.W., G.S., G.F., and C.B.designed experiments. P.W., G.S., S.K., K.Z., and L.H performed experiments. All authors reviewed the manuscript. The authors have declared no competing interest.
Funding AgencyGrant Number
European Research Council (ERC)261286
Swedish Research Council2018-02480
Karolinska InstitutetUNSPECIFIED
Swedish Brain FoundationUNSPECIFIED
Novo Nordisk FoundationUNSPECIFIED
Wenner-Gren FoundationUNSPECIFIED
Record Number:CaltechAUTHORS:20230316-182288000.25
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:120142
Deposited By: George Porter
Deposited On:21 Mar 2023 19:48
Last Modified:21 Mar 2023 19:48

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