For many, the thought of driving down a winding road can induce feelings of nausea and discomfort. But have you ever wondered what causes this unpleasant sensation? Scientists have long been trying to pinpoint the brain cells responsible for motion sickness, and a recent study involving unsuspecting mice has shed some light on the matter.
In this study, mice were placed in a plastic tube and strapped onto a rotating spinner. The purpose of this setup was to observe which neurons in their brains were activated after experiencing motion sickness. As the mice spun around, their body temperature dropped, they avoided food, and they cowered in their cages – all clear signs of the motion sickness they were experiencing.
Based on previous research, the team of scientists led by neuroscientist Pablo Machuca-Márquez decided to focus their attention on a group of neurons known as vestibular nuclei. These neurons are responsible for relaying signals from the ear to the brain and are believed to play a role in motion sickness. By inhibiting different subsets of these neurons and observing the mice’s responses, the researchers hoped to gain a better understanding of the neural mechanisms behind motion sickness.
During the experiment, the researchers discovered that a specific group of vestibular neurons expressing a protein called VGLUT2 played a crucial role in inducing motion sickness. When these neurons were deactivated, the mice no longer experienced motion sickness after being spun around. On the other hand, switching on these neurons without any spinning caused motion sickness-like behaviors in the mice.
Further investigation revealed that neurons expressing both VGLUT2 and a receptor called CCK-A were primarily responsible for the motion sickness behaviors observed in the mice. The researchers mapped the circuitry of these neurons and found that they were connected to an area of the brain known as the parabrachial nuclei. This region of the brain is involved in regulating appetite suppression, body temperature, and lethargy.
If the findings from this mouse study can be extrapolated to humans, it could potentially provide researchers with a clearer target for developing medications to alleviate motion sickness. Most current anti-motion sickness medications work by reducing activity in the brain’s balance system or limiting signals between the brain and gut. However, these medications often come with side effects such as drowsiness and are most effective when taken before the onset of motion sickness.
The discovery of the specific neural pathways and receptors involved in motion sickness could open up new possibilities for developing more targeted and effective medications. By blocking the CCK-A receptors, the researchers were able to alleviate some motion sickness behaviors in the mice. If similar results can be achieved in humans, it could mean a breakthrough in the treatment of motion-induced discomfort.
The search for the source of motion sickness has been a challenging endeavor, but this recent study on mice has provided valuable insights into the neural mechanisms behind this phenomenon. By identifying the specific neurons and receptors involved, researchers now have a potential target for developing more effective medications with fewer side effects. While further research is needed to confirm these findings in humans, the possibility of finding a solution to motion sickness is an exciting prospect that could greatly improve the travel experience for many.
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