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We rarely devote much thought to the act of drinking a glass of water but the decision actually involves a complicated neurological process. Feeling thirsty is part of an elaborate system that regulates the ratio of salt to water in our bodies. Sudden or radical changes in this balance can cause migraines, dizziness or, in extreme cases, death.
Charles Bourque, at the McGill Centre for Research in Neuroscience, spends an awful lot of time thinking about exactly what triggers the sensation of thirst.
Dehydration — caused by lack of water in the body — is a leading cause of emergency room visits. Even more dangerous is a condition called hyponatremia, which is caused by too much water in the body and not enough sodium. (This is an especially serious problem for water-guzzling athletes like marathon runners).
Normally, we avoid drastic changes in our salt-to-water balance because our brains detect small irregularities, setting off a series of neurological events that regulate thirst and release hormones to restore our body's balance. Exactly how our brains perform these tasks remains a mystery, but recent studies in Bourque's laboratory show that a gene called Trpv1 plays a key role.
When the body is dehydrated, the brain shrinks; conversely, with a surplus of water, it expands. A decade ago, Bourque's lab discovered that when brain cells shrink, electrical activity in the brain increases as neurons detect problems with the body's salt-to-water imbalance. They just didn't know how the process worked.
Studies in the United States had indicated that a class of genes — called Trpv genes — might be important to the process. Following this lead, Bourque and McGill graduate students Sorana Ciura and Reza Sharif Naeini bet on a hunch that one particular gene, called Trpv1, might be a key player.
To test Trpv1's importance, the scientists studied mice that had been genetically altered to lack Trpv1. In two different experiments — both recently published in the prestigious scientific journals Nature and The Journal of Neuroscience — the animals' brains didn't respond to sodium imbalances the way a normal animal's would. They didn't know how to recognize the problem or correct it. This is strong evidence that the Trpv1 gene is an important part of the mechanism that detects and corrects changes in salinity, which could have implications for human health.
Bourque speculates that a large percentage of patients with hypertension of unknown origin probably have badly regulated nervous systems that can't detect problems in the salt-to-water balance. And for reasons that aren't entirely understood, elderly people are especially prone to serious and even fatal dehydration because they fail to feel thirsty.
The McGill Trpv1 studies are an exciting step toward understanding how the body's internal sodium regulation works — and why it sometimes fails to work. More studies need to be done but, eventually, researchers may be able to use these findings to develop drugs that restore the thirst mechanism in patients who are now vulnerable to hydration-related illnesses.