NeuronOct 24, 2017

Increased AMPA Receptor Movement in the Brain's Appetite Control Area May Help Natural GLP-1 Reduce Hunger

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 25, 2026

Abstract

Stimulation of GLP-1 afferent fibers within the paraventricular nucleus (PVN) effectively suppresses food intake.

GLP-1-expressing neurons in the hindbrain project to the PVN, which plays a role in regulating food intake.
Activation of GLP-1 receptors in the PVN enhances excitatory signaling in corticotropin-releasing hormone neurons.
This receptor activation triggers a signaling pathway involving protein kinase A, leading to changes in AMPA receptor function.
Depleting GLP-1 receptors in the PVN after birth is linked to increased food intake and obesity.

Simplified

Glucagon-like Peptide 1 (GLP-1)-expressing neurons in the hindbrain send robust projections to the paraventricular nucleus of the hypothalamus (PVN), which is involved in the regulation of food intake. Here, we describe that stimulation of GLP-1 afferent fibers within the PVN is sufficient to suppress food intake independent of glutamate release. We also show that GLP-1 receptor (GLP-1R) activation augments excitatory synaptic strength in PVN corticotropin-releasing hormone (CRH) neurons, with GLP-1R activation promoting a protein kinase A (PKA)-dependent signaling cascade leading to phosphorylation of serine S845 on GluA1 AMPA receptors and their trafficking to the plasma membrane. Finally, we show that postnatal depletion of GLP-1R in the PVN increases food intake and causes obesity. This study provides a comprehensive multi-level (circuit, synaptic, and molecular) explanation of how food intake behavior and body weight are regulated by endogenous central GLP-1. VIDEO ABSTRACT.

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Increased AMPA Receptor Movement in the Brain's Appetite Control Area May Help Natural GLP-1 Reduce Hunger

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