For the first time ever, researchers say they’ve used functional magnetic resonance imaging (fMRI) to uncover the mechanism for short-term thirst and thirst quenching, according to a new article in the journal Nature.
The study authors noted that changes in blood makeup that have previously been thought to regulate all thirst behavior happen slowly, yet humans and other animals can experience rapid development of thirst and rapid quenching of thirst, before any reaction to saltier blood or actual fluid depletion would have time to take place.
“However, most drinking behavior is regulated too rapidly to be controlled by blood composition directly, and instead seems to anticipate homeostatic imbalances before they arise,” the authors wrote.
Before there is an actual dehydration problem, the body seems able to realize dehydration could occur in the future and so mobilizes other mechanisms to induce thirst and then water intake.
So the researchers looked at mice’s brains to look for a secondary explanation. They used fMRIs to look at the circumventricular organs (CVO) of the brain, which the paper points out are the portions of the brain that deal with fluid balances and imbalances in the body. But the quick-fire changes in thirst and drinking behavior the scientists were looking for weren’t apparent in these areas using an fMRI.
The researchers looked specifically at one CVO, called SFO neurons, with in vivo fluorescence.
They found that SFO thirst activators were deactivated within one minute of mice beginning to drink water after being deprived through the night. That shows that actual satiation is not the thing that cuts of the quick-response thirst mechanism, but just the act of starting to drink.
The authors explained that “drinking resets thirst-promoting SFO neurons in a way that anticipates the future restoration of homeostasis. Importantly, this anticipatory feedback provides a mechanism to explain how animals can match ongoing water consumption to the level of physiological need, a longstanding observation that has lacked a clear neural basis.”
Through manipulating the mice’s SFO neurons, the researchers also found that other homeostasis-monitoring sensors throughout the body would override silenced SFO neurons if the body did not appear to have drunk its fill even after the first intake of water, so that the mice (and presumably, humans) would then still continue to drink.
They also found that the colder the water drunk by the mice, the more quickly their SFO thirst neurons appeared to calm down. The mice felt more satiated by cold water than by warm or room-temperature water. Simply putting something cold (even if not a liquid) into a mouse’s mouth helped to show some thirst-quenching responses in the brain. This could explain why “why thirsty rodents will avidly lick cold metal and humans report that sucking on ice chips rapidly relieves thirst,” the study authors wrote.
And they found that eating also activated the SFOs, which is possibly why people and animals tend to drink during meals. The researchers speculated that eating caused the SFOs to anticipate a future change in blood makeup (from the food) and to signal a desire for water before that change even occurred.
All of this means CVOs that focus on thirst brought about by homeostatic change and thirst brought about by anticipating homeostatic change through SFOs work together to regulate behaviors connected to drinking. The study authors were able to find the neural mechanisms for widely observed, almost “common sense” behaviors.
“This convergence provides a straightforward mechanism for the brain to compare the needs of the body with the anticipated effects of ongoing food and water consumption and then adjust behavior pre- emptively. This in turn explains longstanding behavioral observations, including the speed of thirst satiation, the fact that oral cooling is thirst-quenching, and the widespread coordination of eating and drinking,” the study authors wrote.