Abstract
The neuromodulator dopamine is integral to feeding behavior, believed to modulate food pursuit and satiety. Here, we examine how dopamine signaling in the nucleus accumbens changes during consumption as animals transition from hunger to satiety in naturalistic feeding. Dopamine transiently increases during food approach; however, the magnitude of this approach-related increase diminishes across progressive pellet ingestion, reflecting short-term satiation. These approach-related dopamine transients recover during intermeal intervals. Fasting dissociates the regulation of meal size and frequency, reflecting termination and initiation, respectively, with observable differences in dopamine corresponding to changes in meal size but not frequency. Despite substantially decreasing feeding, pharmacological satiation via a glucagon-like peptide-1 (GLP-1) agonist had no impact on average dopamine transients on food approach but abolished the short-term fluctuations related to on-going eating, suggesting that the GLP-1 agonist disengaged or decoupled dopamine from its modulatory role in meal patterning.
Full text
1,203 characters
· extracted from
oa-doi-fallback
· click to expand
Abstract
The neuromodulator dopamine is integral to feeding behavior, believed to modulate food pursuit and satiety. Here, we examine how dopamine and spiny projection neurons (SPNs) signaling in the nucleus accumbens changes during consumption as animals transition from hunger to satiety in naturalistic feeding. Both dopamine and SPNs transiently increase during food approach; however, the magnitude of this approach-related increase diminishes across progressive pellet ingestion, reflecting short-term satiation. Fasting dissociates the regulation of meal size and frequency-- termination and initiation, respectively-- with altered dopamine corresponding to changes in meal size but not frequency. Despite substantially decreasing feeding, pharmacological satiation via a glucagon-like peptide-1(GLP-1) agonist had no impact on dopamine signaling, suggesting that the GLP-1 agonist disengaged or decoupled dopamine from its modulatory role in food seeking.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
↵† Dept. of Neuroscience and Physiology, New York University Grossman School of Medicine, New York, NY
corrected issue with poor resolution on figures.
Text is read by the "Ask this paper" AI Q&A widget below.
Extraction quality varies by source — PMC NXML preserves structure
cleanly, OA-HTML may include some navigation residue, and OA-PDF can
have broken hyphenation. The publisher copy
(via DOI)
is the canonical version.