# Regulation of Pain by Alcohol and Endocannabinoids in the Basolateral Amygdala

> **NIH NIH F31** · LSU HEALTH SCIENCES CENTER · 2020 · $37,373

## Abstract

Abstract
Chronic pain affects approximately 100 million Americans, a number that is projected to increase over the next
several decades. Chronic pain represents a negative affective state that promotes the transition from
recreational, limited intake to alcohol dependence and excessive alcohol drinking. Acutely, alcohol produces
analgesia in humans, and 25% of chronic pain patients and 79% of high-risk alcohol drinkers use alcohol to
manage their pain. We have shown that acute alcohol administration attenuates increased pain sensitivity (or
allodynia) in our rodent model of chronic inflammatory pain, and that the analgesic effects of alcohol may shift
over the course of chronic pain. However, there is a gap in knowledge regarding the neurobiological
mechanisms underlying the analgesic effects of alcohol in the context of chronic pain. The basolateral
amygdala (BLA) plays an important role in various pain processes, including pain chronification and the
regulation of pain-associated negative affect. Chronic pain increases BLA spontaneous and evoked activity
and cFos mRNA expression, and our preliminary data suggest that alcohol dependence and withdrawal
induces a state of increased pain sensitivity due to a similar increase in BLA activity. The endocannabinoid
system (eCB) is well known for mediating analgesia, and we have shown that alcohol withdrawal-induced pain
avoidance behavior is associated with a potential decrease in eCB tone within the BLA. The main research
objective of the current proposal is to investigate the role of BLA activation and endocannabinoid signaling in
the analgesic effects of acute alcohol. The studies outlined in this proposal will test the predictions that: 1)
acute alcohol activates BLA interneurons in the context of chronic inflammatory pain and that activation of
these neurons are necessary for the analgesic effects of alcohol, and 2) that acute alcohol will increase BLA
endocannabinoids and that inhibition of the endocannabinoid catabolic enzyme monoacylglycerol lipase
(MAGL) will rescue increases in pain-like behavior in a manner similar to that of acute alcohol administration.
In addition to filling a gap in knowledge regarding the neurobiology underlying the relationship between chronic
pain and alcohol, this proposal will provide a promising future biomedical science PhD with vital research
training to become an independent scientist in the field of alcohol research.

## Key facts

- **NIH application ID:** 9992675
- **Project number:** 1F31AA028445-01
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Jessica Cucinello-Ragland
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $37,373
- **Award type:** 1
- **Project period:** 2020-08-20 → 2023-08-19

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9992675

## Citation

> US National Institutes of Health, RePORTER application 9992675, Regulation of Pain by Alcohol and Endocannabinoids in the Basolateral Amygdala (1F31AA028445-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9992675. Licensed CC0.

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