Tokyo Institute of Technology or Tokyo Tech scientists recently provided a deeper understanding of neural thirst control.
Their research, which Nature Communications published, specifies that cholecystokinin-medicated water-intake suppression is regulated by a pair of neuronal "thirst-suppressing" sub-populations in the "subfornical organ in the brain," ScienceTechDaily reported, excessive levels of water insistently activate one population, and the other, briefly following water drinking.
Water sustains life here on earth. The first life came from an ancient sea, and since then, almost every species that has been present before, or the present life, relies on the exact balance of salt and water called body-fluid homeostasis or salt homeostasis to survive.
More so, humans can survive for weeks, minus food, but they won't last more than a couple of days, emphasizing the essentiality of this liquid.
'Hyponatremia'
The human body comprises various intricate mechanisms to guarantee we are consuming an adequate amount of water to maintain the homeostasis, which is necessary to survival.
As specified in this research, one of the simple but essential "hacks" is thirst. When the human body is experiencing dehydration during a hot day, noted by a condition known as hypernatremia, the excessive sodium in the body compared to water, the brain is sending signals to the rest of the body, resulting in a craving for a glass of water.
On the other hand, under the hyponatremia condition, where there is more water compared to sodium, water drinking is suppressed. Such neural mechanisms of how this occurs are said to be "a subject of great interest.
The research from Tokyo Tech, led by Professor Masaharu Noda, has performed an extensive study.
Thirst Driven by 'Water Neurons'
In their past research, the researchers found that thirst is driven by what's called the "water neurons" in the brain's subfornical organ or SFO, an area just outside the "blood-brain barrier."
When the body suffers from dehydration, plasma levels of a peptide hormone, also known as "angiotensin II, increase." Such levels are discovered by water neurons' special "angiotensin II 'receptors'" to activate water intake.
In turn, under sodium-depleted circumstances, where there's more water than sodium, these water neurons' activity is blocked by interneurons called "GABAergic."
According to Prof. Noda, the latter control seemed to be reliant on the hormone cholecystokinin or CCK in the SFO. Nonetheless, the CCK-mediated neural instruments underlying water intake's inhibitory control "had not been elucidated, so far."
Now, in their latest research, which Nature Communications published, the study authors discovered more details on this mechanism.
They did a series of experiments, including transgenic mice research, "single-cell dynamics, fluorescence microscopic Ca2 + imaging, and optical and chemogenetic silencing," to discover the neurons found in the SFO.
The study investigators presented several interesting observations. One of the is that CCK was generated in the "SFO itself, by CCK-producing excitatory neurons," which trigger the GABAergic interneurons through their "CCK-B" receptors, leading them to block the water neurons and stop thirst.
Then, they also found two unique subpopulations of the CCK neurons. Group 1, which is the largest population, shows strong and retained activation under the body's excessive water, also known as the Na-depleted condition.
Group 2, on the other hand, is showing quicker and more transient stimulation in response to the intake of water, with the stimulation lasting note exceeding 20 seconds. There are clues of a third group, although these neurons do not exhibit activation in any conditions.
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