If your favorite position when riding in a boat or a car is curled up in a dark corner because you’re queasy, you might want to give thanks for the creatures that underpin much of medical research’s baby steps.
A new study conducted in mice may have solved part of a mystery that has plagued a share of humans since transportation of any sort was invented: motion sickness.
Researchers from the Autonomous University of Barcelona believe they’ve figured out which cells in the brain are responsible for misinterpreting sensory signals from our inner ears, eyes and legs in a way that creates the gut-wrenching malady.
The findings were just released in the journal PNAS, formerly the Proceedings of the National Academy of Sciences.
Cleveland Clinic says motion sickness occurs “when your brain can’t make sense of information sent to your eyes, ears and body. Lots of motion — in a car, airplane, boat or even an amusement park ride — can make you feel queasy, clammy or sick to your stomach. Some people vomit.”
To figure it out, the researchers sent the mice to an amusement park of sorts.
Neurons and spin cycles
ScienceAlert.com describes what the researchers did: “Unsuspecting mice were plopped in a plastic tube, strapped onto a rotating spinner, and sent for a ride, so researchers could pinpoint which neurons lit up after this nausea-inducing merry-go-round.”
Released from the “ride,” the mice crept away, hunkering down, uninterested in food. The researchers said their body temperatures dropped, too — symptoms familiar to those who experience motion sickness.
The scientists wanted to see which brain cells responded to the mismatched signals received, in hopes the information can be used to develop better medication for motion sickness. So they inhibited various subsets of neurons in the vestibular nuclei, a kind of communication hub in the brainstem, before putting the mice back on the ride to see if they got sick again or not.
When they inactivated vestibular neurons that express the VGLUt2 protein, the animals could spin without getting wobbly or sick. They reported that of those vestibular neurons, the cholecystokinin (CCK)-expressing vestibular neurons seems responsible for the ill effects.
When they stimulated dense areas of CCK-A neurons in the brain’s parabrachial nuclei — “an area known to regulate appetite suppression, body temperature and lethargy,” per ScienceAlert.com — some of the motion sickness symptoms returned. “The animals’ body temperature fell and they avoided sugary foods, but they still ate and moved normally, so other connections stemming from vestibular nuclei likely induced those bodily responses to motion sickness,” the article said.
Blocking the CCK-A receptor before the mice were spun alleviated some of the signs of motion sickness.
“Most anti-motion sickness medications work similarly, to reduce activity in the brain’s balance system or limit signals being sent between the brain and gut, to help stop nausea and vomiting,” the article notes.
The question now is whether humans have the same neural pathway. And while the finding’s hopeful, research takes time, so if you’re among the third of humankind that gets motion sick, don’t count on riding that roller coaster with ease any time soon.
Preventing motion sickness now
In the meantime, experts offer some advice to temper the misery. The Centers for Disease Control and Prevention recommends:
- Sitting in the front of the motor vehicle.
- Take a window seat on flights or train rides.
- When you can, lie down, shut your eyes, sleep or stare at the horizon.
- Drink plenty of water, but limit alcohol or caffeine.
- Eat small amounts of food often.
- Don’t smoke. “Even stopping for a short period of time helps,” CDC says.
- Distract yourself.
- Suck flavored lozenges. CDC recommends ginger candy.
- Medicines for motion sickness can also relieve symptoms, but may cause drowsiness. Benadryl, Dramamine and scopolamine are three examples.