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

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

  • 期刊论文

  • 发表日期：

    2025年3月21日

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  • 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

摘要

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.