# Mechanisms of enhanced synaptic drive in basolateral amygdala following stress

> **NIH NIH R21** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2023 · $432,500

## Abstract

Project Summary
Fear conditioning, where an initially neutral warning stimulus becomes associated with an innately aversive
stimulus such as nociceptive electric shock, has proven to be an effective model for the study of learning and
memory processes generally and how learned experiences contribute to anxiety disorders particularly. We
reported that a single experience with a strong stressor leads to a long-term enhancement of fear learning, an
effect we termed Stress-Enhanced Fear Learning (SEFL). Previously, we demonstrated the importance of the
basolateral amygdala (BLA) in SEFL and that SEFL is accompanied by a long-term upregulation of the GluA1
subunit of the AMPA receptor, specifically in the BLA. AMPA receptors mediate normal excitatory neural
transmission. This suggests that SEFL, and perhaps other negative consequences of stress, may be mediated
by alterations in excitatory synaptic transmission. However, the precise mechanisms by which stress alters
fear conditioning are not known. Such knowledge is important to understand how state variables impact
learning and memory processes. Additionally, understanding how stress alters fear learning may point to
translational targets for stress-related disorders. Therefore, we propose a series of studies using amygdala
slice electrophysiology to address this gap in the literature and open the door to future studies determining the
necessary and sufficient mechanisms for SEFL. Our preliminary data using whole-cell recordings indicates that
there is enhanced excitatory drive in the basolateral amygdala following SEFL-inducing stress. In this
exploratory application we propose to use BLA slice electrophysiology to achieve two aims. First to identify the
specific inputs to the BLA that carries this enhanced excitatory drive. The second is to identify the molecular
mechanisms responsible for this change in excitatory synaptic transmission focusing on the possibility that an
abnormal form of neural plasticity underlies these maladaptive changes.

## Key facts

- **NIH application ID:** 10723781
- **Project number:** 1R21MH134158-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Michael S Fanselow
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $432,500
- **Award type:** 1
- **Project period:** 2023-09-10 → 2025-09-09

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10723781

## Citation

> US National Institutes of Health, RePORTER application 10723781, Mechanisms of enhanced synaptic drive in basolateral amygdala following stress (1R21MH134158-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10723781. Licensed CC0.

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