# Vagal-hypothalamic modulation of alcohol intake

> **NIH NIH R01** · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · 2024 · $495,905

## Abstract

Abstract
Alcohol use disorder (AUD) is the third leading cause of preventable death in the U.S. and 32.6 million adults
have AUD. AUD etiology is highly diverse and current treatment strategies for AUD have high rates of relapse
(40 to 60%). Therefore, identifying novel factors facilitating development of AUD is critical, and expansion of
the `tool-box' beyond current behavioral and pharmacological targets is required for development of novel
effective treatments. A critical gap that hampers discovery of novel AUD treatment is the lack of studies
examining the interaction of the brain and body during various stages of the disease. The vagus nerve is the
main conductor of brain-body signals and previous clinical and preclinical evidence, as well as our preliminary
data, suggest dysfunction of vagus nerve activity is a driver of AUD development and relapse risk.
Furthermore, our preliminary data shows that a selective gastric vagotomy (VX) results in increased alcohol
intake and preference in rodent models and is associated with alterations in paraventricular (PVN)
hypothalamic neurocircuits. Therefore, we propose to use a combination of behavioral, electrophysiological,
molecular, histological and viral transgenic techniques to test the novel hypothesis that disruptions of the
gastric vagus nerve activity may increase alcohol preference via selective down-regulation of PVN oxytocin
function. As a corollary to this, we will investigate whether targeting PVN oxytocin neurons may rescue VX-
induced increases in alcohol preference. Specific Aim 1 will test the hypothesis that VX will increase alcohol
reward (preference and seeking) and alters PVN gene expression. Specific Aim 2 then will test the hypothesis
that activation of PVN oxytocin neurons will rescue increased alcohol preference following VX. Identifying
specific brain targets and mechanisms underlying the beneficial effects of healthy vagal activity to reduce
alcohol preference, thus reducing motivation for alcohol consumption, could further aid development of both
novel pharmacological and non-pharmacologic AUD interventions.

## Key facts

- **NIH application ID:** 10852316
- **Project number:** 1R01AA031470-01
- **Recipient organization:** PENNSYLVANIA STATE UNIV HERSHEY MED CTR
- **Principal Investigator:** ANDRAS HAJNAL
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $495,905
- **Award type:** 1
- **Project period:** 2024-09-25 → 2027-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10852316

## Citation

> US National Institutes of Health, RePORTER application 10852316, Vagal-hypothalamic modulation of alcohol intake (1R01AA031470-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10852316. Licensed CC0.

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