When our body needs to be hydrated, a whole mechanism is set in motion, guided by “water neurons”.
- When our body experiences dehydration, the brain sends signals to the rest of the body to hydrate through water neurons that fuel thirst in the subfornical organ (SFO) of the brain.
- This mechanism is also activated in the event of hyponatremia, when there is more water than sodium, this time to cut the desire for water.
Humans cannot survive more than a few days without hydration. Our body mass is made up of 60% water. To be certain that we consume the necessary quantity of water to survive, several mechanisms are triggered to maintain homeostasis, the regulatory process by which our body ensures that a constant level of all body fluids is maintained. our body. One of the most important mechanisms is the feeling of thirst. A team of Japanese researchers from the Tokyo Institute of Technology has studied this mechanism in depth and identified “water neurons” responsible for its activation. They presented their findings in NatureCommunications November 10.
Activate the need for water, switch off this need
When our body experiences dehydration, the brain sends signals to the rest of the body to hydrate. These signals are powered by the famous “water neurons” that feed thirst into the subfornical organ (SFO) of the brain, a region just outside the blood-brain barrier. When the body is dehydrated, plasma levels of a peptide hormone called angiotensin II increase. These levels are sensed by special receptors in water neurons to stimulate water consumption.
This mechanism is also activated in the event of hyponatremia, when there is more water than sodium. The water neurons will activate to regulate this level and cut the desire to consume water. The activity of the water neurons is then suppressed by “GABAergic” interneurons. “This latter control appeared to be dependent on the hormone cholecystokinin (CCK) in the subfornical organ (SFO) of the brain. However, the CCK-mediated neural mechanisms underlying the inhibitory control of water intake had not yet been elucidated.”, continues Professor Masaharu Noda who led the team of researchers.
Control alcohol consumption?
The researchers conducted a series of experiments on transgenic mice to explore the neurons of the subfornical organ (SFO). They observed that cholecystokinin (CCK) was produced in the SFO itself by specific neurons that activate GABAergic interneurons via their “CCK-B” receptors, causing them to suppress water neurons and inhibit the thirst. They also discovered that there are two distinct subpopulations of these CCK neurons. The first, which is the largest population, shows a strong and sustained activation in the case where the body contains more water than sodium. The second shows a more rapid and transient activation in response to water intake, the activation lasting no more than 20 seconds. There are also hints of a third group, but these neurons do not show activation in either condition.
“Since CCK has long been known to be a gastrointestinal hormone, these findings open up many possibilities, the most exciting being the likelihood of negative feedback control of alcohol consumption based on water-sensing cues. from the oropharynx or gastrointestinal tract”, rejoices Professor Noda.
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