Feeling itchy? Scientists may have discovered the mechanism of how our body initiates an itch.
A study using mice conducted at the National Institutes of Health showed that a molecule called natriuretic polypeptide b (Nppb) may be the culprit behind that pesky itch. This specific molecule sets off a chain reaction, leading to what our brain perceives as an itch, or what is medically known as pruritus.
"Our work shows that itch, once thought to be a low-level form of pain, is a distinct sensation that is uniquely hardwired into the nervous system with the biochemical equivalent of its own dedicated land line to the brain," senior author Mark Hoon, a scientist at the National Institute of Dental and Craniofacial Research, part of the NIH, said in a press release.
The study was published May 23 in Science.
Researchers began the study by looking at signaling areas on specific neurons, or nerve cells, that have a molecule called TRPV1. These particular neurons are tasked with monitoring external sensations like temperature and pain. Scientists previously believed that these cells were responsible for controlling both itch and pain, and the signal strength of the itch was dependent how strong the stimuli was.
Hoon's team looked at the main neurotransmitters -- chemical messengers that neurons release when they are triggered that send signals to other nearby nerve cells -- that TRPV1 neurons produce in mice. They then looked to see which of the neurotransmitters, which included Nppb, was in charge of sending signals about sensation. Nppb had previously been identified as a molecule released by the heart to control sodium and blood pressure, but this study showed it was also released by the spine.
By removing Nppd from some mice, the researchers confirmed the molecule's involvement in itching.
"We tested Nppb for its possible role in various sensations without success," lead author Santosh Mishra, a researcher in Hoon's laboratory, said in the press release. "When we exposed the Nppb-deficient mice to several itch-inducing substances, it was amazing to watch. Nothing happened. The mice wouldn't scratch."
Nppb specifically fits into a specific kind of spinal chord nerve cell, which then sends a signal throughout the body's central nervous system. The mice stopped scratching even though they were in situations that would make them itchy once Nppb or the nerve cell was removed, but their other sensory functions remained intact. This also meant that Nppb was necessary to make the body respond to itchy items.
Previously some scientists thought there wasn't an initial trigger like Nppb that started the itch sensation process, because it would be too difficult considering all the different cells that processed the sensation. Other theorists suggested a neurotransmitter called GRP may be the itch trigger. This study showed that GRP was involved in sending itch signals throughout the nervous system, but it only kicked in after Nppb started everything in motion.
More needs to be done to figure out how the process works in humans and how we can stop chronic itching conditions. Hoon pointed out to TIME that getting rid of the neurotransmitter in a person might lead to blood pressure problems, so it isn't exactly an easy cure.
"The larger scientific point remains," Hoon explained in a press release. "We have defined in the mouse the primary itch-initiating neurons and figured out the first three steps in the pruritic pathway. Now the challenge is to find similar biocircuitry in people, evaluate what's there, and identify unique molecules that can be targeted to turn off chronic itch without causing unwanted side effects. So, this is a start, not a finish."
Malcolm Rustin, a dermatologist with the British Association of Dermatologists, told the BBC that the study was "interesting," and that it is very important that medications to combat itch be developed.
"In patients with eczema, the first symptom is itch. There is debate if you have itch, damage the skin barrier and let allergens in, it becomes a vicious circle," he said.