Glucagon-Like Peptide-1 Receptor Signaling in the Lateral Parabrachial Nucleus Contributes to the Control of Food Intake and Motivation to Feed

Apr 1, 2014Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

Signaling of a hunger-regulating receptor in the brain’s lateral parabrachial area helps control eating and food motivation

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Abstract

Activation of GLP-1 receptors in the lateral parabrachial nucleus (lPBN) reduced food intake and motivation to work for food.

GLP-1-producing neurons in the nucleus tractus solitarius connect directly to the lPBN.
Pharmacological activation of GLP-1 receptors in the lPBN resulted in decreased food intake.
Blocking GLP-1 receptors in the lPBN led to increased food intake.
Activation of GLP-1 receptors in the lPBN lowered the motivation to work for food in a progressive ratio task.
These findings suggest that the lPBN plays a significant role in GLP-1 receptor-mediated control of food intake and reward.

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Central glucagon-like peptide-1 receptor (GLP-1R) activation reduces food intake and the motivation to work for food, but the neurons and circuits mediating these effects are not fully understood. Although lateral parabrachial nucleus (lPBN) neurons are implicated in the control of food intake and reward, the specific role of GLP-1R-expressing lPBN neurons is unexplored. Here, neuroanatomical tracing, immunohistochemical, and behavioral/pharmacological techniques are used to test the hypothesis that lPBN neurons contribute to the anorexic effect of central GLP-1R activation. Results indicate that GLP-1-producing neurons in the nucleus tractus solitarius project monosynaptically to the lPBN, providing a potential endogenous mechanism by which lPBN GLP-1R signaling may exert effects on food intake control. Pharmacological activation of GLP-1R in the lPBN reduced food intake, and conversely, antagonism of GLP-1R in the lPBN increased food intake. In addition, lPBN GLP-1R activation reduced the motivation to work for food under a progressive ratio schedule of reinforcement. Taken together, these data establish the lPBN as a novel site of action for GLP-1R-mediated control of food intake and reward.

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Glucagon-Like Peptide-1 Receptor Signaling in the Lateral Parabrachial Nucleus Contributes to the Control of Food Intake and Motivation to Feed

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