Children’s Nutrition Research Center Staff Publications

Language

English

Publication Date

4-7-2025

Journal

Nature Metabolism

DOI

10.1038/s42255-025-01234-9

PMID

40119169

Abstract

Motion sickness is associated with thermoregulation and metabolic control, but the underlying neural circuitry remains largely unknown. Here we show that neurons in the medial vestibular nuclei parvocellular part (MVePC) mediate the hypothermic responses induced by motion. Reactivation of motion-sensitive MVePC neurons recapitulates motion sickness in mice. We show that motion-activated neurons in the MVePC are glutamatergic (MVePCGlu), and that optogenetic stimulation of MVePCGlu neurons mimics motion-induced hypothermia by signalling to the lateral parabrachial nucleus (LPBN). Acute inhibition of MVePC-LPBN circuitry abrogates motion-induced hypothermia. Finally, we show that chronic inhibition of MVePCGlu neurons prevents diet-induced obesity and improves glucose homeostasis without suppressing food intake. Overall, these findings highlight MVePCGlu neurons as a potential target for motion-sickness treatment and obesity control.

Keywords

Animals, Motion Sickness, Mice, Body Temperature Regulation, Neurons, Obesity, Vestibular Nuclei, Male, Mice, Inbred C57BL, Behavior, Animal, Optogenetics

Published Open-Access

yes

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