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

> **NIH NIH R03** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2021 · $50,256

## Abstract

Summary of Parent Grant
Drugs that target glucagon-like peptide 1 receptor (GLP-1R) systems 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 brain 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. The parent grant proposal will test the functional requirements of GLP-1Rs neurons in
mediating its activation, the endogenous role of CeA GLP-1Rs in food intake, and the role of CeA GLP-1Rs in
mediating the actions of peripherallyadministered agonists.
The parent grant will characterize: the functional role of CeA GLP-1Rs in regulating neural activity and neural
responses to peripherally applied GLP-1R agonists (Aim 1) and 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 (Aim 2). Specifically, we will utilize in vivo Ca2+ fiber
photometry in combination with 1) local deletion of CeA GLP-1Rs and 2) local CeA administration of GLP-1R
agonists. Site-specific genetic deletion of CeA GLP-1Rs in combination with longitudinal assessment of
feeding using miniaturized feeding devices adapted for operant feeding (Aim 2).
Functionally, we hypothesize that CeA GLP-1Rs are required for the neurophysiological effects of
peripherally administered GLP-1R agonists on the CeA and that direct activation of CeA GLP- 1Rs is
sufficient to induce robust changes in CeA neural activity in vivo. Behaviorally, we hypothesize that CeA
GLP-1Rs drive motivation and appetitive behavior for palatable food and that deletion of these receptors will
partially suppress the effects of peripherally administrated GLP-1R agonists on binge-like food intake. The
significance of the parent proposal is to discern the contribution of the brain’s endogenous GLP-1R system
to better inform more effective treatments for obesity and type II diabetes.
The overarching hypothesis is that CeA GLP-1Rs function endogenously to constrain large volume food
intake, motivation for palatable food, and are partially required for the anorexigenic effects of peripheral
GLP-1R agonists on food intake.

## Key facts

- **NIH application ID:** 10414577
- **Project number:** 3R03DK129561-01S1
- **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:** $50,256
- **Award type:** 3
- **Project period:** 2021-06-01 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10414577

## Citation

> US National Institutes of Health, RePORTER application 10414577, Functional and Behavioral Characterization of Central Amygdala Glucagon Like Peptode-1 Receptors (3R03DK129561-01S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10414577. Licensed CC0.

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