ArticleProceedings of the National Academy of Sciences of the United States of America2023
Vestibular CCK signaling drives motion sickness-like behavior in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Gingerol-Rich Extract Derived fromInternational journal of molecular sciences · 2026Article
- Review
- Dysfunctional LHX6 pallido-subthalamic projections mediate epileptic events in a mouse model of Leigh syndrome.The Journal of clinical investigation · 2025Article
- Sensory signals for nausea.Trends in neurosciences · 2025Review
- Functional and imaging anomalies of the vestibular system in motion sickness: a clinical observation study.BMC medical imaging · 2025Observational
- Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice.Nature metabolism · 2025Article
- Neural pathways of nausea and roles in energy balance.Current opinion in neurobiology · 2025Review
- Effects of two kinds of vestibular function training on reducing motion sickness in college students.Frontiers in neurology · 2025Article
- Gravitational change-induced alteration of the vestibular function and gene expression in the vestibular ganglion of mice.The journal of physiological sciences : JPS · 2024Article
- On labyrinthine function loss, motion sickness immunity, and velocity storage.Frontiers in neurology · 2024Article
- Evaluating proxies for motion sickness in rodent.IBRO neuroscience reports · 2023Article
- A New Vestibular Stimulation Mode for Motion Sickness With Emphatic Analysis of Pica.Frontiers in behavioral neuroscience · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
Travel can induce motion sickness (MS) in susceptible individuals. MS is an evolutionary conserved mechanism caused by mismatches between motion-related sensory information and past visual and motion memory, triggering a malaise accompanied by hypolocomotion, hypothermia, hypophagia, and nausea. Vestibular nuclei (VN) are critical for the processing of movement input from the inner ear. Motion-induced activation of VN neurons recapitulates MS-related signs. However, the genetic identity of VN neurons mediating MS-related autonomic and aversive responses remains unknown. Here, we identify a central role of cholecystokinin (CCK)-expressing VN neurons in motion-induced malaise. Moreover, we show that CCK VN inputs onto the parabrachial nucleus activate
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.