# Traumatic stress increases alcohol drinking via endocannabinoid disinhibition of basolateral amygdala

> **NIH NIH R01** · LSU HEALTH SCIENCES CENTER · 2020 · $369,409

## Abstract

Project Summary
Humans with post-traumatic stress disorder (PTSD) are more likely to develop alcohol use disorder (AUD) than
the general population, and AUD is the most commonly co-occurring mental health disorder in humans with
PTSD. These conditions, separately and combined, affect millions of American, cause millions of deaths
worldwide, and cost society billions of dollars. This proposal will examine individual differences in traumatic
stress effects on specific brain circuits in male and female alcohol drinkers, and will manipulate those circuits to
test their role in post-stress escalation of alcohol drinking. Here, we focus specifically on amygdala disinhibition
and endocannabinoid signaling, but we will collect blood and brain samples that allow for subsequent analysis
of predictive biomarkers, as well as follow-up experiments in alternate brain circuits.
This project falls within the scope of the NIAAA mission to support biological and behavioral research
underlying addictive behaviors. More importantly, the current proposal addresses the research objectives
outlined in RFA-AA-17-016 by assessing alcohol drinking in a well characterized animal model of PTSD,
determining the association of pre-stress alcohol drikning with the development of post-stress escalation of
alcohol drinking, systematically testing the effect of sex on post-stress escalation of alcohol drinking, identifying
neurobiological processes that underlie the transition to post-stress escalation of alcohol drinking, and
identifying neurobiological targets for potential treatment of alcohol abuse in PTSD patients. Specifically, this
application proposes the use of rat models to examine the neurobiology underlying stress-induced escalation
of alcohol drinking in male and female animals. This application proposes the use of behavioral,
electrophysiology, biochemistry, and molecular biology techniques to identify brain circuits altered by traumatic
stress in subsets of alcohol drinkers, and to directly test the role of those circuits in escalated alcohol drinking
after stress. The overall goals of the proposed work are to test the role of 1) amygdala disnihibition and 2) brain
endocannabinoid signaling in traumatic stress-induced escalation of alcohol drinking in a stress-susceptible
subpopulation.

## Key facts

- **NIH application ID:** 9985672
- **Project number:** 5R01AA026531-04
- **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:** $369,409
- **Award type:** 5
- **Project period:** 2017-09-15 → 2022-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9985672

## Citation

> US National Institutes of Health, RePORTER application 9985672, Traumatic stress increases alcohol drinking via endocannabinoid disinhibition of basolateral amygdala (5R01AA026531-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9985672. Licensed CC0.

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