# Impact of social drive on social fear learning and amygdala function during development

> **NIH NIH F32** · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · 2020 · $65,310

## Abstract

PROJECT ABSTRACT
Heightened fear responding and social dysfunction are commonly seen in individuals suffering from debilitating
fear-related disorders, such as Post-Traumatic Stress Disorder (PTSD). Exposure-based treatments are often
ineffective at minimizing robust fear responses. Adolescents are especially prone to the development of fear-
and stress-related disorders as well as symptom persistence following therapeutic interventions. Understanding
developmental differences in the persistence of fear could therefore lead to more targeted, age-appropriate
interventions. Directly experienced traumatic events are significant triggers in anxiety disorders and PTSD.
However, adolescent observation of trauma or abuse also increases risk of diagnosis. The impact of observed
trauma depends on the social sensitivity of the observer, which is high during adolescence. This social sensitivity
combined with ongoing brain maturation may produce adolescent vulnerabilities for these disorders. The
investigation of factors that contribute to behavioral and biological changes across the lifespan is critical for a
thorough understanding of adaptive fear responding. The goal of this proposal is to identify the factors that
contribute to socially learned fear in adults and adolescents, and how these factors lead to persistent fear
behavior during adolescence. We will use social fear learning (SFL), which requires social interaction and social
inference, and requires amygdala circuits to learn and retain fear. We hypothesize that changes in social
sensitivity and amygdala circuitry from adolescence to adulthood contribute to differences in how SFL is learned
and retained. We will test this general hypothesis in two specific aims. Aim 1 will determine how changes in
social drive between adults and adolescents impact SFL and retention as well as cortico-amygdala synaptic
strength using whole cell electrophysiology. Aim 2 will target how socially-inferred fear responding may change
with acute manipulations in observed fear using optogenetics, and the impact this has on synaptic strength in
the amygdala using whole cell electrophysiology. These results will provide information for new therapeutic
strategies to understand the developmental differences in how fear is retained through changes in social drive.

## Key facts

- **NIH application ID:** 10020193
- **Project number:** 5F32MH122092-02
- **Recipient organization:** ROSALIND FRANKLIN UNIV OF MEDICINE & SCI
- **Principal Investigator:** Nicole Christine Ferrara
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $65,310
- **Award type:** 5
- **Project period:** 2019-09-16 → 2022-09-15

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10020193

## Citation

> US National Institutes of Health, RePORTER application 10020193, Impact of social drive on social fear learning and amygdala function during development (5F32MH122092-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10020193. Licensed CC0.

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