# Functional and Behavioral Characterization of Central Amygdala Glucagon Like Peptode-1 Receptors

> **NIH NIH R03** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2021 · $111,375

## Abstract

Project Summary
Drugs that target the glucagon-like peptide 1 receptor (GLP-1R) system are commonly prescribed for the
treatment of type II diabetes. Unfortunately, we do not yet fully understand how these drugs work on targets in
the central nervous system or how brain GLP-1Rs regulate eating behaviors. In this proposal we will characterize
the functional role of GLP-1Rs in the central amygdala (CeA) using neural circuit, genetic, and behavioral
approaches in laboratory mice. In Aim 1, we will use fiber photometry of GCaMP7 in the CeA in combination with
1) local deletion of CeA GLP-1 and 2) local CeA administration of GLP-1R agonists to determine the functional
role of CeA GLP-1Rs in regulating neural activity and neural responses to peripherally applied GLP-1R agonists.
In Aim 2, we will use site-specific genetic deletion of CeA GLP-1Rs in combination with high precision,
longitudinal assessment of feeding using miniaturized feeding devices that can be used in the mouse homecage
and adapted for operant feeding. Using this technology, we will measure appetitive and consummatory behavior
under free or operant conditions throughout the light cycle over several weeks. We will also determine if CeA
GLP-1Rs are required for the anorexigenic effects of peripherally administered GLP-1R agonists using two
separate paradigms: fasting-induced refeed and intermittent access to high fat diet. Using these two binge-like
eating paradigms will peripherally administer Exendin-4, a potent GLP-1R agonist, in the presence or absence
of CeA GLP-1Rs. We hypothesize that CeA GLP-1Rs are required for the neurophysiological effects of
peripherally administered GLP-1R agonists on the CeA and that activation of CeA GLP-1Rs is sufficient to induce
robust changes in CeA neural activity in vivo. Behaviorally, we hypothesize that CeA GLP-1Rs constrain
motivation and appetitive behavior for palatable food, and that deletion of these receptors will partially suppress
the effects of peripheral GLP-1R agonists on binge-like food intake. Over the long-term we hope to understand
the contribution of the brain’s endogenous GLP-1R system that may inform more effective treatments for obesity
and type II diabetes.

## Key facts

- **NIH application ID:** 10286169
- **Project number:** 1R03DK129561-01
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** James Andrew Hardaway
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $111,375
- **Award type:** 1
- **Project period:** 2021-06-01 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10286169

## Citation

> US National Institutes of Health, RePORTER application 10286169, Functional and Behavioral Characterization of Central Amygdala Glucagon Like Peptode-1 Receptors (1R03DK129561-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10286169. Licensed CC0.

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