Transcriptionally defined amygdala subpopulations play distinct roles in innate social behaviors

Author:

Lischinsky Julieta E.ORCID,Yin Luping,Shi Chenxi,Prakash Nandkishore,Burke Jared,Shekaran Govind,Grba Maria,Corbin Joshua G.,Lin DayuORCID

Abstract

AbstractSocial behaviors are innate and supported by dedicated neural circuits, but the molecular identities of these circuits and how they are established developmentally and shaped by experience remain unclear. Here we show that medial amygdala (MeA) cells originating from two embryonically parcellated developmental lineages have distinct response patterns and functions in social behavior in male mice. MeA cells expressing the transcription factor Foxp2 (MeAFoxp2) are specialized for processing male conspecific cues and are essential for adult inter-male aggression. By contrast, MeA cells derived from the Dbx1 lineage (MeADbx1) respond broadly to social cues, respond strongly during ejaculation and are not essential for male aggression. Furthermore, MeAFoxp2 and MeADbx1 cells show differential anatomical and functional connectivity. Altogether, our results suggest a developmentally hardwired aggression circuit at the MeA level and a lineage-based circuit organization by which a cell’s embryonic transcription factor profile determines its social information representation and behavioral relevance during adulthood.

Funder

U.S. Department of Health & Human Services | NIH | National Institute of Mental Health

Leon Levy Foundation

NYU Dean’s Undergraduate Research Funds NYU Collegiate Research Initiative

NYU Dean’s Undergraduate Research Funds

U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse

Caroline Fredricka Holdship Charitable Trusts through the PNC Charitable Trust Grant Review Commission

G. Harold and Leila Y. Mathers Foundation

U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development

Brain Initiative

Publisher

Springer Science and Business Media LLC

Subject

General Neuroscience

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