# Developmental and circuit mechanisms for innate social behaviors in the medial amygdala

> **NIH NIH K99** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2022 · $130,545

## Abstract

Project Summary
 Innate social behaviors are crucial for survival, thus shared across animal species. In humans, psychiatric
disorders with deficits in social interactions include autism spectrum disorders and conduct disorder. Both of
these conditions can be observed during early child development and have been associated with amygdala
dysfunction. However, there is still a lack of understanding of the circuitry and developmental mechanisms for
the generation of social behaviors; topics I aim to study in the long-term. To do so, I focus on the medial
amygdala (MeA) as it is a region that has been implicated in both the processing of social olfactory cues and
the generation of social motor actions in mice. The goal of this project is to uncover the neuronal circuitry for
the sensory and motor processing of social behaviors, specifically aggression, and the developmental
mechanisms for their establishment in male and female mice. I will take a developmental approach to study
aggression by taking advantage of my previously characterized MeA neuronal subpopulation, marked by the
expression of the embryonic and postnatal transcription factor Foxp2. MeA Foxp2+ cells are molecularly and
physiologically distinct from other developmentally-defined subpopulations in the region. I present a central
hypothesis in which there are sexually dimorphic differences in the sensory processing of social information
arising during postnatal development in the MeA, resulting in specific downstream functional circuits. I will take
a holistic approach and study sex-specific differences at distinct developmental trajectories and under different
environmental conditions. In Aim 1 (K99), I will investigate the cellular responses and functions of MeA Foxp2+
cells in female mice during aggression and other social behaviors through the use of fiber photometry and
chemogenetic tools. In Aim 2 (K99), I will establish the MeA Foxp2+ cells downstream projections in male and
female mice to uncover sex-specific differences in the circuits for aggression. In Aim 3 (R00), I will study the
developmental mechanisms for the generation of these circuits at distinct time-points pre-and post-puberty. I will
also investigate how the circuit may be modified by early life adverse experiences. In the mentored phase of the
award, I will complete a training plan to develop and strengthen technical skills for circuit dissection in adult and
juvenile mice. By integrating a diverse set of convergent techniques, including multi-fiber photometry, circuit
mapping and genetically encoded sensors across developmental time-points in male and female mice, this
project will greatly advance our understanding of the developmental mechanisms for the establishment of
sexually dimorphic circuits for social behaviors.

## Key facts

- **NIH application ID:** 10442591
- **Project number:** 5K99MH127295-02
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Julieta E Lischinsky
- **Activity code:** K99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $130,545
- **Award type:** 5
- **Project period:** 2021-07-01 → 2023-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10442591

## Citation

> US National Institutes of Health, RePORTER application 10442591, Developmental and circuit mechanisms for innate social behaviors in the medial amygdala (5K99MH127295-02). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10442591. Licensed CC0.

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