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Parabrachial CGRP Neurons Control Meal Termination.
Carlos A Campos1, Anna J Bowen1, Michael W Schwartz2
1Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.
Cell Metabolism
|May 12, 2016
Summary
Calcitonin gene-related peptide (CGRP) neurons in the lateral parabrachial nucleus control meal termination. Inhibiting these neurons increases meal size and reduces satiety, revealing a key interaction between hunger and satiety circuits.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Neurobiology
Background:
- The lateral parabrachial nucleus (PBel) relays visceral signals contributing to anorexia.
- Calcitonin gene-related peptide (CGRP) expressing neurons in the PBel were previously shown to inhibit feeding during illness.
Purpose of the Study:
- To investigate the role of CGRP neurons in normal feeding behavior and satiety.
- To elucidate the interaction between AgRP neurons and CGRP neurons in regulating feeding.
Main Methods:
- Functional inactivation of CGRP neurons in mice.
- Assessment of meal size and frequency.
- Investigation of satiety peptide effects.
- Optogenetic stimulation of AgRP fibers innervating the PBel.
Main Results:
- Inactivation of CGRP neurons increased meal size and reduced sensitivity to satiety peptides.
- CGRP neurons are directly innervated by orexigenic AgRP neurons.
- AgRP stimulation of PBel inhibited CGRP neurons, delaying satiation and promoting hyperphagia.
Conclusions:
- CGRP neurons play a crucial role in terminating meals.
- These neurons act as a downstream mediator for AgRP-driven feeding.
- A critical node where hunger and satiety circuits interact to control feeding behavior has been identified.
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