Neurobiology of Thirst: Neural Mechanisms that Control Hydration
Scientists at the Tokyo Institute of Technology (Tokyo Tech) provide deeper insights into neural thirst control. Their study published recently in Nature Communications indicates that cholecystokinin-mediated water-intake suppression is controlled by two neuronal ‘thirst-suppressing’ sub-populations in the subfornical organ in the brain; one population is persistently activated by excessive water levels, and the other, transiently after drinking water.
Water sustains life on earth. The first life originated in an ancient sea, and since then, nearly every species that has existed in the past or lives today depends on the exact balance of salt and water (~145 mM; called body-fluid homeostasis or salt homeostasis) for survival. Humans can go weeks without food but will not last more than a few days without water, stressing the importance of this liquid.
The human body has several intricate mechanisms to make sure we consume an appropriate amount of water for maintaining the homeostasis, which is requisite to survival. One of these simple but key “hacks,” is thirst. When the body experiences dehydration on a hot day (noted by the excess of sodium in the body compared to water, a condition called hypernatremia), the brain sends “signals” to the rest of the body, making us crave the tall glass of water. On the other hand, under a condition called hyponatremia, where there is a more water than sodium, we suppress water drinking. The neural mechanisms of how this happens are a subject of great interest.
A team of researchers from Tokyo Institute of Technology, headed by Prof Masaharu Noda, have conducted extensive research into this. In their previous studies, they identified that thirst is driven by the so-called “water neurons” in the subfornical organ (SFO) of the brain, a region just outside the blood-brain barrier. When the body is dehydrated, the plasma levels of a peptide hormone called angiotensin II increase. These levels are detected by special angiotensin II “receptors” of water neurons to stimulate water intake. In turn, under sodium-depleted conditions (where there is more water than sodium), the activity of these water neurons is suppressed by “GABAergic” interneurons. “The latter control appeared to be dependent on the hormone cholecystokinin (CCK) in the SFO. However, the CCK-mediated neural mechanisms underlying the inhibitory control of water intake had not been elucidated so far,” states Prof Noda.