Circuits in the brain finely tune the amount of water you consume to maintain the delicate balance of water and salts that keeps your body ticking.
Now, a study conducted by researchers at the University of Washington in Seattle, US, has pinpointed a cluster of neurons that help monitor water consumption, and could protect against over-drinking, a potentially dangerous activity to which amateur athletes and the elderly are sometimes prone.
One of the hallmarks of these neurons: they can be switched on by the hormone oxytocin.
Oxytocin is often simplistically referred to as the “love hormone” because its ability to promote trust and bonding between people. But oxytocin is somewhat of a hormonal Swiss army knife, capable of controlling a wide variety of bodily functions and behaviours.
It can quell fear and anxiety, yet it can also increase less savoury social emotions of jealousy and Schadenfreude.
Oxytocin is also responsible for uterine contractions during birth, and the letdown reflex in breasts that feeds the baby through infancy.
Less well known is its role in controlling how much we drink and eat. To investigate this particular role, the researchers homed in on cells that respond to oxytocin in a brain region known to be involved in consumption – the parabrachial nucleus (PBN). This small cluster of cells is located in the brainstem, an ancient region that controls some of our most basic functions such as breathing.
The researchers genetically engineered mice with PBN cells harbouring oxytocin receptors that could be switched on or off. They also fixed tiny microscopes to the heads of the mice, allowing a close-up view of the neural circuits in action in awake mice.
Under normal conditions, when mice were dehydrated, the PBN oxytocin receptors were silent. But these cells burst into action as soon as the mice started to drink water.
“As they start drinking, more and more of [the neurons] switch on,” says lead author Philip Ryan, now at the Florey Institute of Neuroscience and Mental Health in Melbourne.
“There’s probably a point where there’s so many of them switched on that it tells the mouse to stop drinking.”
Lapping at an empty bottle or consuming a mousey meal-replacement shake failed to activate the neurons. This indicates that the circuit is specifically involved in responding to water, not to the licking motion, nor to consumption in general.
When the neurons were artificially switched on, mice sensed they had enough fluid in their system, and so didn’t drink water when dehydrated. And when inactivated, the mice upped their salt intake.
Fluid balance can go awry in medical conditions such as heart failure, kidney failure and liver cirrhosis, and controlling the urge to overdrink can be excruciating.
Tapping into this neural circuit could be a way of helping these patients, says Ryan.
Dyani Lewis is a freelance science journalist based in Melbourne, Australia.
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