Oxytocin is well known for its role as the ‘trust hormone’, as well as aiding delivery and breast feeding when babies are born, but is less well known for its role in regulating the body’s fluid levels and saltiness.
Brain cells containing the oxytocin receptor, located in the ancient reptilian part of the brain, stop us drinking too much salty water when thirsty or eating that last chip when we know we can’t bear any more saltiness.
The brain is extremely good at preventing us from drinking too much water, which can lead to lethal consequences like severe brain swelling. These brain circuits are also important for patients with heart or kidney damage, who can end up with too much fluid in their bodies, doing even further damage to patient’s vital organs.
Intriguingly, these oxytocin brain circuits regulating salt may also be involved in anxiety and drug addiction, suggests new research, opening the way for potential therapies.
Dr Philip Ryan, from the Florey Institute of Neuroscience and Mental Health in Melbourne, used an elegant combination of chemical, genetic and imaging experiments to tease out the role of oxytocin receptor cells in the brain circuits controlling our hunger, thirstiness and desire for salt – all crucial pathways that arose during our evolutionary struggle to survive.
Dr Ryan first showed that oxytocin receptor cells were located in an area of the hindbrain called the parabrachial nucleus or PBN for short. The PBN has previously been implicated in regulating how much we eat, drink and seek salt.
“What hasn’t been clear up to this point was the precise groups of PBN cells responsible for these behaviours, and how. Using genetically engineered mice we turned the oxytocin receptor cells on and off, and showed the cells reduced fluid intake, but had no effect on food intake,” Dr Ryan says.
Then, examining the oxytocin receptor cells after the mice had been denied salt or fluid, Dr Ryan saw the cells switch on again only after the mice had rebalanced their need for salt or water. The cells actually protected the body against excessive fluid or salt intake after a period of dehydration or salt deprivation.
Finally, Dr Ryan examined other parts of the brain that could activate the oxytocin receptor cells. When stimulated, these cells were part of a chain reaction, reducing fluid intake by the mice.
“Excitingly, given the brain regions involved in the oxytocin circuit, we think these cells are going to play a role in more complex behaviours, like anxiety. Also, given the role of salt satisfaction in the same reward pathway that gets hijacked by addictive drugs, this research opens up potential avenues for new addiction treatments” says Dr Ryan.
The findings were published in prestigious journal Nature Neuroscience and the work was performed in the laboratory of the ‘godfather of genetically engineered mice’, Professor Richard Palmiter, at the University of Washington in Seattle.