# Rodent model of alcohol related hyperalgesia

> **NIH NIH R01** · OREGON HEALTH & SCIENCE UNIVERSITY · 2021 · $346,500

## Abstract

Project Summary
Over a hundred million of Americans suffer from chronic pain and over ten million of Americans suffer from
alcohol abuse or dependence. There is a bidirectional relationship between chronic pain and alcohol
dependence. Thus, alcohol dependence is a major predictor of severity of chronic pain, and people with
chronic pain conditions are more likely to use alcohol for pain relief. Unfortunately, a mechanistic
understanding of alcohol-related pain sensitivity is lacking. Our studies have identified increased pain
sensitivity in mice during withdrawal from voluntary alcohol self-administration. Consumption of alcohol in these
mice reversed mechanical hypersensitivity produced by alcohol withdrawal. The increased pain sensitivity in
mice undergoing withdrawal is consistent with increased pain in alcohol-dependent patients. In addition, we
found increased pain sensitivity in control “bystander” mice housed in the same room as mice undergoing
alcohol withdrawal. The social transfer of hyperalgesia from mice undergoing withdrawal to the bystander mice
involved olfactory cues. Such social transfer of hyperalgesia could affect "co-dependent" family members of
alcoholic patients. Immunohistochemical analysis revealed differential activation of dorsomedial hypothalamus,
anterior cingulate and anterior insular cortex in these animals. We hypothesize that the identified brain regions
are differentially involved in alcohol withdrawal-induced hyperalgesia and socially-transferred hyperalgesia.
The goal of this proposal is to address this hypothesis and further characterize the phenomena of alcohol
withdrawal- and social transfer-induced hyperalgesia. This goal will be achieved in three Specific Aims: Aim 1
will further characterize the phenomenon of hyperalgesia in alcohol withdrawing and bystander mice by
examining whether the observed thermal hyperalgesia is exaggerated in female bystander mice, involves
negative affective states, anxiety or stress responses, or coexists with depression-like behaviors. Aim 2 will
test whether alcohol-induced activation of neuronal populations within dorsomedial hypothalamus is necessary
and sufficient for regulation of pain sensitivity and alcohol drinking behavior in mice. Aim 3 will test whether
alcohol withdrawal and social transfer-induced activation of neurons of anterior cingulate and/or insula are
necessary and sufficient for regulation of pain sensitivity.

## Key facts

- **NIH application ID:** 10189448
- **Project number:** 5R01AA025024-05
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Mary Magdalen Heinricher
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $346,500
- **Award type:** 5
- **Project period:** 2017-08-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10189448

## Citation

> US National Institutes of Health, RePORTER application 10189448, Rodent model of alcohol related hyperalgesia (5R01AA025024-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10189448. Licensed CC0.

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