Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/151045
Title: A distinct parabrachial-to-lateral hypothalamus circuit for motivational suppression of feeding by nociception
Authors: Phua, Siew Cheng
Tan, Yu Lin
Kok, Alison Maun Yeng
Senol, Esra
Chiam, Christine Jin Hui
Lee, Chun-Yao
Peng, Yanmin
Lim, Auriel Theodora Jacobea
Mohammad, Hasan
Lim, Jing-Xuan
Fu, Yu
Keywords: Science::Medicine
Issue Date: 2021
Source: Phua, S. C., Tan, Y. L., Kok, A. M. Y., Senol, E., Chiam, C. J. H., Lee, C., Peng, Y., Lim, A. T. J., Mohammad, H., Lim, J. & Fu, Y. (2021). A distinct parabrachial-to-lateral hypothalamus circuit for motivational suppression of feeding by nociception. Science Advances, 7(19), eabe4323-. https://dx.doi.org/10.1126/sciadv.abe4323
Project: 1530700142
Journal: Science Advances 
Abstract: The motivation to eat is not only shaped by nutrition but also competed by external stimuli including pain. How the mouse hypothalamus, the feeding regulation center, integrates nociceptive inputs to modulate feeding is unclear. Within the key nociception relay center parabrachial nucleus (PBN), we demonstrated that neurons projecting to the lateral hypothalamus (LHPBN) are nociceptive yet distinct from danger-encoding central amygdala–projecting (CeAPBN) neurons. Activation of LHPBN strongly suppressed feeding by limiting eating frequency and also reduced motivation to work for food reward. Refined approach-avoidance paradigm revealed that suppression of LHPBN, but not CeAPBN, sustained motivation to obtain food. The effect of LHPBN neurons on feeding was reversed by suppressing downstream LHVGluT2 neurons. Thus, distinct from a circuit for fear and escape responses, LHPBN neurons channel nociceptive signals to LHVGluT2 neurons to suppress motivational drive for feeding. Our study provides a new perspective in understanding feeding regulation by external competing stimuli.
URI: https://hdl.handle.net/10356/151045
ISSN: 2375-2548
DOI: 10.1126/sciadv.abe4323
Rights: © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles

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