# The Role of Amygdala Outputs in Stress-Induced Escalation of Alcohol Drinking

> **NIH NIH F32** · LSU HEALTH SCIENCES CENTER · 2020 · $33,723

## Abstract

PROJECT SUMMARY
 Alcohol use disorder (AUD) is a major public health problem that affects millions of Americans. Traumatic
stress disorders are highly co-morbid with AUD and can contribute to the development of AUD. Rat studies in
our lab have shown that traumatic (predator odor) stress produces stress-induced conditioned place avoidance
and escalated alcohol drinking in a subset of stressed rats, termed Avoiders, recapitulating the individual
differences in stress reactivity seen in humans. Comparisons of predator odor stress-induced neuroadaptations
in Avoider and Non-Avoider rats have revealed that corticotropin-releasing factor (CRF) signaling via CRF-1
receptors (CRFR1) in the central amygdala (CeA) represents one mechanism by which predator odor stress
alters behavior. However, it is not known whether stress-induced plasticity in CRF-CRFR1 signaling in CeA
mediates stress-induced escalation of alcohol drinking in Avoider rats, nor is it known whether altered CRFR1
signaling in CeA mediates post-stress behavior by gating the activity of specific CeA outputs. Here, I propose to
test the role of 1) CeA CRF-CRFR1 signaling, 2) CeA projections to lateral hypothalamus (LH), and 3) CeA
CRFR1+ projections to LH, in stress-induced escalation of alcohol drinking and reward in Avoider rats. Our
overarching hypothesis is that CeALH CRFR1+ neurons mediate traumatic stress-induced escalation of
alcohol drinking and reward. I will use a combination of immunohistochemistry, chemogenetics, and anatomical
techniques to test this hypothesis. In Specific Aim 1, I will test the hypothesis that Avoider rats will show greater
activation of CeALH CRFR1+ neurons than Non-Avoider and Control rats after predator odor stress. In Specific
Aim 2, I will test the hypotheses that 1) inhibition of CeALH CRFR1+ neurons will attenuate stress-induced
escalation of alcohol drinking and alcohol reward in Avoider rats, and 2) stimulation of CeALH CRFR1 neurons
will increase alcohol drinking and alcohol reward in stress-naïve rats. I will use the newly-engineered male and
female CRFR1:Cre rats for all experiments. The proposed work will provide information regarding brain circuit
mediators and potential drug targets for the treatment of co-morbid AUD and traumatic stress disorders. In
addition, this project will provide important training to a promising young alcohol neuroscientist.

## Key facts

- **NIH application ID:** 10264773
- **Project number:** 5F32AA027145-02
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Marcus Matthias Weera
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $33,723
- **Award type:** 5
- **Project period:** 2019-08-14 → 2021-02-13

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10264773

## Citation

> US National Institutes of Health, RePORTER application 10264773, The Role of Amygdala Outputs in Stress-Induced Escalation of Alcohol Drinking (5F32AA027145-02). Retrieved via AI Analytics 2026-06-24 from https://api.ai-analytics.org/grant/nih/10264773. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*