Chuck Bednar for redOrbit.com – Your Universe Online
Scientists from the Howard Hughes Medical Institute at Columbia University in New York have discovered the circuitry in the brain that regulates thirst in mice.
The culprits, they report in a paper published Monday in the journal Nature, are two different sets of cells located in a region of the brain known as the subfornical organ (SFO). When the first is switched on, it led the mice to begin drinking immediately, whether they needed to or not. Activating the second suppressed the urge to drink, regardless of dehydration levels.
“We view the SFO as a dedicated circuit that has two elements that likely interact with each other to maintain the perfect balance,” explained Charles Zuker, lead investigator on the study and a researcher in the department of biochemistry and molecular physics at HHMI. “So you drink when you have to and you don’t drink when you don’t need to.”
The circuit ensures the correct fluid intake to maintain blood pressure, electrolyte balance, and cell volume. The search for these brain-based regulators grew out of research conducted by Zuker and his colleagues on the multiple pathways devoted to salt – how the brain senses it and makes sure it’s only appealing in moderation.
The search began in the SFO because it shows signs of increased activity in dehydrated animals. Since the SFO is located outside the blood-brain barrier, it has direct contact with body fluids, meaning that the cells could have the ability to detect electrolyte balance in those fluids.
Oka wanted to discover if there were any specific cells in the SFO that triggered drinking behaviors. By analyzing genetic markers, he found three distinct types of cells in the SFO: excitatory cells, inhibitory cells, and supporting cells called astrocytes.
“If these neurons really mediated key aspects in driving the motivation to drink, then their activation should trigger active drinking, irrespective of the degree of fluid satiety, and if you silence these populations, you should suppress the motivation to drink, even if you are extraordinarily thirsty,” Zuker said.
In order to test those predictions, Oka introduced a light-sensitive protein into cells in the SFO. This allowed the scientists to selectively activate those cells in the mice. Using blue light from a laser, they activated the excitatory SFO cells in hydrated mice, and found that the mouse almost immediately began desiring water.
“There is an animal that is happily wandering around, with zero interest in drinking,” said Zuker. “You activate this group of excitatory neurons, and it just beelines to the water spout. As long as the light is on, that mouse keeps on drinking.”
The mice expressed zero interest in other types of fluids, but would heartily consume water for prolonged periods of time, the study authors said. In fact, some of the creatures were drank up to eight percent of their body weight, or equal to about 1.5 gallons of water for the average human.
Zuker called the findings “very exciting,” and added that the circuit “informs and directs the mouse into a complex program of actions and behaviors: ‘I’m thirsty. I need to identify a source of water. I have to go where the water is. I have to begin to consume that water and I have to continue until this signal is suppressed.’”
Next, they tested the effect of the SFO’s inhibitory neurons. When activated in thirsty mice, the creatures reduced their water intake by approximately 80 percent. Activating those inhibitors did not affect the animal’s interest in food or salt, indicating a different set of neurons for those needs.
Zuker noted that the behavior of the mice was “independent of learning, experience, or context,” suggesting that the thirst-regulating circuit is hard-wired into the brain. Their findings reveal that the brain has an innate circuit which can switch an animal’s water-drinking behavior on and off, and most likely functions as a center for thirst control in the mammalian brain.
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