Recently Tokyo Institute of Technology or Tokyo Tech scientists recently gave a deeper understanding of neural thirst control.
Their research, published by Nature Communications, points out that water intake with cholecystokinin is regulated by a pair of neuronal subunits “quenching thirst” in the “subfornical organ in the brain, ”Reported ScienceTechDaily, excessive water levels consistently activate one population, and the other, shortly after drinking water.
Water sustains life here on earth. The first life came from an ancient sea, and since then, almost all species that have been present before, or the present life, are dependent on the true balance of salt. and water is called homeostasis liquid or salt homeostasis to survive.
In addition, people can live for weeks, without food, but they do not last more than a day or two, confirming the importance of this liquid.
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The researchers found that thirst is driven by what are known as the ‘water neurons’ in the subfornical organ of the brain or SFO, an area just outside the ‘blood-brain barrier.’
‘Hyponatremia’
There are several complex ways in which the human body can ensure that we consume enough water to maintain the homeostasis, which is essential for survival.
As pointed out in this research, thirst is one of the simplest but necessary “hacks”. When the human body gets hydrated in a hot day, characterized by a condition called hypernatremia, the excess sodium in the body compared to water, the brain sends signals to the rest of the body , and as a result there is a great grip for a glass of water.
On the other hand, under the condition of hyponatremia, where there is more water compared to sodium, drinking water is suppressed. Cloud devices like this are said to be “a topic of great interest.
The research from Tokyo Tech, led by Professor Masaharu Noda, has been extensively studied.
Thirst led by Water Neurons
In their previous research, the researchers found that thirst is driven by what are known as the “water neurons” in the subfornical organ of the brain or SFO, an area just outside a “blood clot” -eanchan. “
When the body suffers from dehydration, plasma levels of the peptide hormone, also known as “angiotensin II,” increase. These levels are detected by specific “angiotensin II receptors” for water neurons. to introduce.
At the same time, in sodium-depleted conditions, where there is more water than sodium, the activity of these water neurons is inhibited by interneurons called “GABAergic.”
According to Professor Noda, the latter control appeared to be due to the hormone cholecystokinin or CCK in the SFO. Nonetheless, the CCK-centric cloud instruments controlled by water intake control have not been “clarified, to date.”
Now, in their latest research, published by Nature Communications, the authors of the study found more details about this approach.
They performed a series of experiments, including transgenic mouse study, “single-cell dynamics, Ca2 + fluorescence microscopic imaging, and optical and chemogenetic disruption,” to determine the neurons found in the SFO.
Researchers presented a number of interesting observations. One of the CCKs generated in the “SFO itself, by CCK excitatory neurons,” is that the GABAergic interneurons stimulate through their “CCK-B” receptors, directing them to block and stop the water neurons on thirst.
Then, they also found two specific subpopulations of the CCK neurons. Group 1, the largest population, exhibits strong and conserved activity under excess body water, also known as Na-depleted condition.
Group 2, on the other hand, exhibits a faster and more immobile stimulus in response to the incoming water, with the lasting note lasting more than 20 seconds. Signals are from a third group, although these neurons do not exhibit activity under any circumstances.
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