Chips, chips, popcorn – whatever your preference, we all know that salt is a key part of many tasty foods. But eating too much salt poses potential health risks and can lead to cardiovascular and cognitive disorders. Caltech researchers have now identified neurons that cause and dispel salt cravings in the mouse brain. The results are an entry point into the regulation of sodium cravings in humans.
The work was done in the laboratory of Yuki Oka, assistant professor of biology and Chen Scholar. An article describing the research appeared online on March 27, before being published in the newspaper. Nature. Oka is an affiliate faculty member of the Tianqiao Institute of Neuroscience and Chrissy Chen in Caltech.
Sodium – an ion present in table salt – plays a vital role in various body functions, such as cardiovascular activity, fluid balance and nerve signaling. In every animal species, the body regulates and strictly maintains sodium levels. Because animals can not create sodium metabolically themselves, ions must be ingested from external food sources. When the body lacks sodium, the brain triggers specific appetite signals that result in sodium consumption. Although the mechanisms of these appetite signals are not well understood, a team of researchers has discovered a small population of neurons in the posterior mouse brain that controls the drive for sodium consumption.
Under the guidance of Sangjun Lee, a graduate student, the team used genetic tools to manipulate the activity of these neurons so that they could be stimulated by light. The researchers observed that artificial stimulation of these neurons forced the mice to lick a piece of rock salt several times, even when their bodies were completely saturated with sodium.
Next, the researchers measured the activity of these neurons while the mice ate sodium. A few seconds after the sodium hit the tongue of the animal, the activity of sodium-appetite neurons was inhibited. However, a direct infusion of sodium into the stomach of these mice did not suppress neural activity. This neural suppression did not occur either when the sodium receptors on the tongue were pharmacologically blocked. Taken together, research shows that oral sodium signals, probably mediated by the taste system, are needed to inhibit the neurons of the sodium appetite.
"The desire to eat salt is the way your body tells you that your body lacks sodium," Oka says. "Once the sodium is consumed, the body needs time to absorb it completely. So it's worth noting that the taste of sodium is enough to calm the activity of neurons in the body. Salt appetite, which means much more important in regulating body functions than simply transmitting external information to the brain. "
Interestingly, in many species, including humans, sodium intake may stimulate the desire to eat even more. In her future work, Oka and her collaborators would like to understand how the neurons of sodium's appetite are modulated over time. Answering this question can open avenues to help people with health problems consume less sodium in their diet.
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Material provided by California Institute of Technology. Original written by Lorinda Dajose. Note: Content can be changed for style and length.