Motion sickness (MS) is a prevalent and debilitating vestibular disorder with limited therapeutic options, yet the cortical mechanisms governing individual susceptibility remain elusive. Using a biaxial rotation mouse model, we investigated the role of the anterior cingulate cortex (ACC) in MS by integrating morphology, calcium imaging, electrophysiology, cell ablation, chemogenetics, and optogenetics....
✦ The floor
Discussion
Signed responses from readers of the wire.
No actionable change for audiologists or vestibular clinicians at this time; this is animal-model neuroscience that may inform future pharmacological targets for motion sickness but requires human validation.
Identifying a cortico-vestibular circuit for motion sickness susceptibility opens a potential new pathway for targeted therapies beyond current antihistamine and anticholinergic treatments.
- 01Glutamatergic neurons in the anterior cingulate cortex (ACC) modulate vestibular processing relevant to motion sickness.
- 02A cortico-vestibular circuit is proposed as a mechanism linking higher brain function to balance/nausea responses.
- 03Findings are from an animal model; human translation is uncertain.
- 04Published in Neurochemistry International; primarily relevant to vestibular neuroscience researchers.
- 05Could eventually guide drug development targeting central vestibular pathways.
Anterior cingulate cortex glutamatergic neurons modulate motion sickness susceptibility via a cortico-vestibular circuit.
studypartially supported- PMID
- 42843764
- DOI
- 10.1016/j.neuint.2026.106271.
- Journal
- Neurochemistry International
- Publication type
- research_article
- Evidence level
- 4
- Population
- Animal model (species not specified in abstract)
- Intervention
- Manipulation of ACC glutamatergic projection neurons (e.g., chemogenetic or lesion approaches)
- Comparator
- Control animals without ACC manipulation
Primary outcomes
Motion sickness susceptibility; Cortico-vestibular circuit activity