Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice

Longlong Tu; Xing Fang; Yongjie Yang; Meng Yu; Hailan Liu; Hesong Liu; Na Yin; Jonathan C. Bean; Kristine M. Conde; Mengjie Wang; Yongxiang Li; Olivia Z. Ginnard; Qingzhuo Liu; Yuhan Shi; Junying Han; Yi Zhu; Makoto Fukuda; Qingchun Tong; Benjamin Arenkiel; Mingshan Xue; Yang He; Chunmei Wang; Yong Xu

doi:10.1038/s42255-025-01234-9

Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice

Longlong Tu
, Xing Fang
, Yongjie Yang
, Meng Yu
, Hailan Liu
, Hesong Liu
, Na Yin
, Jonathan C. Bean
, Kristine M. Conde
, Mengjie Wang
, Yongxiang Li
, Olivia Z. Ginnard
, Qingzhuo Liu
, Yuhan Shi
, Junying Han
, Yi Zhu
, Makoto Fukuda
, Qingchun Tong
, Benjamin Arenkiel
, Mingshan Xue

Yang He, Chunmei Wang, Yong Xu

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

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 (MVePC^Glu), and that optogenetic stimulation of MVePC^Glu 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 MVePC^Glu neurons prevents diet-induced obesity and improves glucose homeostasis without suppressing food intake. Overall, these findings highlight MVePC^Glu neurons as a potential target for motion-sickness treatment and obesity control.

Original language	English (US)
Article number	101237
Pages (from-to)	742-758
Number of pages	17
Journal	Nature Metabolism
Volume	7
Issue number	4
DOIs	https://doi.org/10.1038/s42255-025-01234-9
State	Published - Apr 2025
Externally published	Yes

Bibliographical note

Publisher Copyright:
© The Author(s), under exclusive licence to Springer Nature Limited 2025.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1038/s42255-025-01234-9

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Tu, L., Fang, X., Yang, Y., Yu, M., Liu, H., Liu, H., Yin, N., Bean, J. C., Conde, K. M., Wang, M., Li, Y., Ginnard, O. Z., Liu, Q., Shi, Y., Han, J., Zhu, Y., Fukuda, M., Tong, Q., Arenkiel, B., ... Xu, Y. (2025). Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice. Nature Metabolism, 7(4), 742-758. Article 101237. https://doi.org/10.1038/s42255-025-01234-9

Tu, L, Fang, X, Yang, Y, Yu, M, Liu, H, Liu, H, Yin, N, Bean, JC, Conde, KM, Wang, M, Li, Y, Ginnard, OZ, Liu, Q, Shi, Y, Han, J, Zhu, Y, Fukuda, M, Tong, Q, Arenkiel, B, Xue, M, He, Y, Wang, C & Xu, Y 2025, 'Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice', Nature Metabolism, vol. 7, no. 4, 101237, pp. 742-758. https://doi.org/10.1038/s42255-025-01234-9

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title = "Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice",

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.",

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AU - Liu, Hesong

AU - Yin, Na

AU - Bean, Jonathan C.

AU - Conde, Kristine M.

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AU - Ginnard, Olivia Z.

AU - Liu, Qingzhuo

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AU - Han, Junying

AU - Zhu, Yi

AU - Fukuda, Makoto

AU - Tong, Qingchun

AU - Arenkiel, Benjamin

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AU - He, Yang

AU - Wang, Chunmei

AU - Xu, Yong

PY - 2025/4

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N2 - 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.

AB - 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.

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Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice

Abstract

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