# Role of Neuropeptides in Stress-Induced Escalation of Alcohol Drinking

> **NIH NIH R01** · LSU HEALTH SCIENCES CENTER · 2020 · $330,750

## Abstract

Traumatic stress disorders affect millions of Americans and cost the U.S. billions of dollars annually. Alcohol use
disorder (AUD) affects ~12% of the world population, contributing to >2.5 million deaths per year in the U.S. and
costing the U.S. $220 billion annually. Post-traumatic stress disorder (PTSD) triples the risk for developing AUD.
PTSD and AUD increase mortality in humans by increasing the incidence of chronic disease. PTSD diagnoses
are also associated with higher incidence of chronic pain in humans. Current treatment strategies for PTSD,
AUD and chronic pain are sub-optimal. The goal of the proposed work is to 1) test traumatic stress effects on
the activity of molecularly identified neurons in central amygdala (CeA) that project to reward/aversion and pain
centers and 2) test the role of specific CeA projection cells in mediating stress effects on alcohol reward/aversion
and sensory nociception & pain avoidance.
We will use an established animal model of traumatic stress in which rats are exposed to predator odor (i.e.,
bobcat urine), then indexed for avoidance of the odor-paired context; this model is predicated on the fact that
avoidance is a hallmark symptom of PTSD in humans. Similar to what is seen in humans with traumatic stress
disorders, our published data show that Avoiders exhibit escalation of alcohol drinking and hyperalgesia after
stress. We will use this model to test circuit and molecular mechanisms mediating traumatic stress effects on
behavior. Specific Aim 1 tests the prediction that traumatic stress activates LH-projecting CeA CRFR1+ cells
and inhibits vlPAG-projecting CeA CRFR1+ cells in alcohol-drinking male and female CRFR1:cre rats. Specific
Aim 2 tests the prediction that inhibition of LH-projecting CeA CRFR1+ cells will reverse stress-induced increases
in alcohol self-administration and reductions in alcohol aversion in male and female CRFR1:cre rats. Specific
Aim 3 tests the prediction that activation of vlPAG-projecting CeA CRFR1+ cells will reverse stress-induced
hyperalgesia and increases in pain avoidance in male and female CRFR1:cre rats. We will use brain slice
electrophysiology, anatomical tract-tracing, retrograde neural labeling and molecular biology techniques,
combined with circuit-based and pharmacological approaches to test stress effects on behavior in CRFR1:cre
rats developed by our lab.

## Key facts

- **NIH application ID:** 10073019
- **Project number:** 2R01AA023305-07
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Nicholas Warren Gilpin
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $330,750
- **Award type:** 2
- **Project period:** 2014-08-05 → 2025-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10073019

## Citation

> US National Institutes of Health, RePORTER application 10073019, Role of Neuropeptides in Stress-Induced Escalation of Alcohol Drinking (2R01AA023305-07). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10073019. Licensed CC0.

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