Motion sickness affects a significant portion of the population, yet its underlying brain circuits remain largely unexplored. A recent study published in Nature Metabolism by researchers from Baylor College of Medicine, the University of Texas Health Science Center at Houston, and the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital sheds light on a new brain circuit involved in motion sickness that may also play a role in regulating body temperature and metabolic balance. These findings could pave the way for novel approaches to treating obesity.
Dr. Yong Xu, professor of pediatrics - nutrition and associate director for basic sciences at the USDA/ARS Children’s Nutrition Research Center at Baylor, explained how his interest was piqued by Dr. Longlong Tu's proposal to explore the brain circuits associated with motion sickness. "When Dr. Longlong Tu, a postdoctoral fellow in my lab, proposed to investigate the brain circuits involved in motion sickness, a condition for which he is highly susceptible, I was not very excited about the idea because it’s not one of the main interests of my lab," Xu stated. "However, I became more interested and supported Tu’s idea when he explained the emerging evidence suggesting a link between motion sickness and metabolic balance, which is one of my research interests."
The research utilized mouse models to examine how the brain regulates metabolism related to obesity. Although mice do not vomit like humans when experiencing motion sickness, both species show hypothermia when subjected to similar stimuli. This allowed researchers to create a mouse model measuring core body temperature and activity under motion stimuli conditions.
Their findings revealed that motion activates glutamatergic neurons in the medial vestibular nucleus parvocellular part (MVePCGlu) of the brain. These neurons are crucial for mediating thermal adaptations due to motion. The team confirmed their model by demonstrating that anti-nausea drug scopolamine prevents hypothermia induced by motion sickness.
"We further studied this motion sickness circuit by inhibiting the MVePCGlu neurons in the absence of motion stimuli," Xu said. "Inhibiting these neurons led to an increase in body temperature along with increased physical activity." This suggests that chronic inhibition might lead to higher energy expenditure.
Exploring further, they found that mice with inhibited MVePCGlu neurons consumed more food but gained less weight while showing better glucose tolerance and insulin sensitivity—traits linked with improved health outcomes. Xu noted these results underscore "the underappreciated function of the brain’s vestibular system in metabolic balance" and suggested potential unconventional targets for obesity treatment.
For first author Tu, this research offers hope for developing better medications for those suffering from his condition.
Contributors included Xing Fang, Yongjie Yang, Meng Yu among others affiliated with Baylor College of Medicine and other institutions involved.
The study received funding support from several grants including those from NIH (P01DK113954), USDA/CRIS (51000-064-01S), McKnight Foundation as well as an American Heart Association Postdoctoral Fellowship (2020AHA000POST000204188).
