Glucagon-Like Peptide 1 Receptors in Nucleus Accumbens Affect Food Intake

Oct 14, 2011The Journal of neuroscience : the official journal of the Society for Neuroscience

Food intake influenced by glucagon-like peptide 1 receptors in the brain's reward area

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Abstract

GLP-1 injected into the NAc core significantly reduced food intake in rats at 1, 2, and 24 hours posttreatment.

NAc GLP-1 receptors are associated with the suppression of feeding behavior.
Activation of GLP-1 receptors in the NAc core, but not the NAc shell, influences food intake.
Endogenous stimulation of NAc core GLP-1 receptors may help limit food consumption.
NAc core administration of GLP-1 did not induce a conditioned taste aversion, indicating the anorexic effect is not due to nausea.
Increased c-Fos expression in the NAc core suggests heightened neuronal activity following GLP-1 injection.

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Central glucagon-like peptide 1 receptor (GLP-1R) stimulation suppresses food intake, and hindbrain GLP-1 neurons project to numerous feeding-relevant brain regions. One such region is the nucleus accumbens (NAc), which plays a role in reward and motivated behavior. Using immunohistochemical and retrograde tracing techniques in rats, we identified a robust projection from GLP-1 neurons in the nucleus of the solitary tract to the NAc. We hypothesized that activation of NAc GLP-1Rs suppresses feeding. When injected into the NAc core of rats at doses subthreshold for effect when administered to the lateral ventricle, GLP-1 significantly reduced food intake relative to vehicle at 1, 2, and 24 h posttreatment. The same doses had no effect when injected into the NAc shell. NAc core treatment with ventricle-subthreshold doses of the GLP-1R antagonist exendin (9-39) caused significant hyperphagia at 2 h posttreatment, suggesting that endogenous stimulation of NAc core GLP-1Rs plays a role in limiting food intake. It has been suggested that GLP-1 can cause nausea, but we found that NAc core administration of GLP-1 did not cause a conditioned taste aversion to saccharin, suggesting that the anorexic effect of NAc core GLP-1 is not caused by malaise. Finally, we observed that NAc core injection of GLP-1 significantly increased c-Fos expression in the NAc core. We conclude that that GLP-1Rs in the NAc play a physiologic role in food intake control, and suggest that the GLP-1 projection to NAc core may link satiation signal processing in the hindbrain with forebrain processing of food reward.

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Glucagon-Like Peptide 1 Receptors in Nucleus Accumbens Affect Food Intake

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