Diabetes and Vascular Disease

SAT-616 - Functional Dissociation of VTA and CeA GLP-1R Neurons in Feeding Control

Saturday, June 13, 2026

9:30 AM - 4:30 PM CT

Late-Breaking Poster Presenter(s)

GM

Gulsun Memi, Sr., PhD

Postdoctoral Researcher
University of Virginia
Charlottesville, Virginia, United States

Co-Author(s)

CG

Chloe Guo, n/a

Grad Student
University of Virginia
Charlottesville, Virginia, United States
TG

T Bugra Gungul, n/a

Grad Student
University of Virginia
Charlottesville, Virginia, United States
OL

Orien DA Li, n/a

Undergrad Student
University of Virginia
Charlottesville, Virginia, United States
KM

Karan Malik, n/a

Undergrad Student
University of Virginia
Charlottesville, Virginia, United States

Senior Author/Primary Investigator(s)

AG

Ali D. Guler, n/a

Principal Investigator
University of Virginia
Charlottesville, Virginia, United States

Glucagon-like peptide-1 receptor (GLP-1R) signaling is a key regulator of feeding and a major therapeutic target for obesity. While GLP-1 receptor agonists suppress food intake, the role of endogenous GLP-1R neurons across distinct phases of feeding remains unclear. Here, we investigated how GLP-1R neurons in the ventral tegmental area (VTA) and central amygdala (CeA) encode anticipatory, sensory, and post-ingestive phases of feeding.
To dissociate feeding phases, we used three paradigms: pellet feeding (anticipatory/sensory), intraoral infusion (sensory), and gastric infusion (post-ingestive). Using fiber photometry to monitor GCaMP activity in freely behaving mice, we recorded real-time dynamics of GLP-1R neurons in VTA and CeA across nutritive and aversive feeding conditions.
VTAGLP-1R neurons showed consistent activation during pellet consumption, suggesting a role in reward-related and consummatory processing. In contrast, CeAGLP-1R neurons exhibited heterogeneous, bidirectional, and context-dependent responses across paradigms. CeA activity varied across feeding paradigms and stimulus conditions. These findings support a functional dissociation in which VTAGLP-1R neurons encode motivational drive (“appetite”), whereas CeAGLP-1R neurons integrate interoceptive and aversive signals to evaluate and constrain intake (“satiety”).

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