# Physiological consequences of alcohol exposure on CRF 1 neurons in the nucleus tractus solitarius

> **NIH NIH F32** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2022 · $53,521

## Abstract

Abstract
Alcohol use disorder (AUD) is a highly prevalent chronically relapsing disorder characterized by increased
alcohol (EtOH) intake, inability to control consumption, and a negative emotional state during withdrawal.
These behaviors are mediated by cellular and circuit adaptations, which can lead to changes in neuronal
structure and function. One key neuroadaptation involves activation of the corticotropin releasing factor (CRF)
system, a peptide released widely throughout the brain in response to stress. CRF signaling through the CRF1
receptor (CRF1) is associated with increased stress reactivity, anxiety-like behavior, and excessive drinking.
Indeed, polymorphisms in Crhr1 (the gene encoding CRF1) are associated with binge drinking, emotionality,
and risk for developing an AUD. A majority of the research concerning AUDs and CRF1 has focused on the
prefrontal cortex and amygdala, while other areas such as the brainstem are much less well-studied. Located
in the caudal medulla, the nucleus tractus solitarius (NTS) is an autonomic center containing an abundance of
CRF1 receptors. While chronic EtOH drinking has been shown to increase activity of NTS neurons, little is
known about the role of specific NTS subpopulations, most notably CRF1 neurons, in this effect. In this
proposal, we will use male and female CRF1:cre: tdTomato rats and established models of voluntary EtOH
intake combined with a cellular electrophysiological approach. In Aim 1, I will determine the effects of acute
EtOH on excitability and synaptic transmission in CRF1NTS neurons from male and female CRF1:cre: tdTomato
rats. In Aim 2, I will examine the changes in excitability and synaptic transmission in CRF1NTS neurons in male
and female CRF1:cre: tdTomato rats following chronic voluntary EtOH drinking. In Aim 3, I will examine the
effect of chemogenetic manipulation of CRF1NTS neurons on voluntary EtOH drinking in male and female
CRF1:cre: tdTomato rats. Together, these experiments will reveal how CRF1NTS neurons are differentially
impacted by acute and chronic EtOH exposure and how CRF1NTS neurons contribute to alcohol drinking.
Collectively, the results of these studies will advance our understanding of the sex-specific consequences of
alcohol exposure on defined subpopulations in the brainstem and how those subpopulations contribute to
behaviors associated with AUD.

## Key facts

- **NIH application ID:** 10537984
- **Project number:** 1F32AA030493-01
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **Principal Investigator:** Sema Quadir
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $53,521
- **Award type:** 1
- **Project period:** 2022-12-01 → 2023-09-01

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10537984

## Citation

> US National Institutes of Health, RePORTER application 10537984, Physiological consequences of alcohol exposure on CRF 1 neurons in the nucleus tractus solitarius (1F32AA030493-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10537984. Licensed CC0.

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