What Causes Us to Itch? Scientists May Have Found the Clues

According to a new scientific study done on mice published in the May 24 edition of Science, the sensation of itching is hardwired into our nervous systems, and can be traced to a small molecule known as known as natriuretic polypeptide b (Nppb) that is released in the spinal cord, US News reports.

Researchers believe "that detection of itch starts in neurons with fibers that extend to the skin," according to Science News. They measured which chemicals the neurons with skin fibers produced the most in mice, opening up a potential "molecular window" to understanding itching in humans.

Humans and mice share similar nervous systems, so researchers concluded that similar processes likely occur in humans. They say the Nppb molecule triggers a signal that passes through the central nervous system, and their findings may help develop treatments for chronic itch conditions such as eczema and psoriasis. 

"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 landline to the brain," study senior author Mark Hoon, a scientist at the U.S. National Institute of Dental and Craniofacial Research, said in an institute news release. 

In the study, researchers first identified the signaling compoments on nerve cells that contain a molecule known as TRPV1, cells that help monitor our external conditions such as temperature and pain. The authors of the study screened the molecule Nppb while examining how these nerve cells recognize various sensations in the body.

"We tested Nppb for its possible role in various sensations without success," said study lead author Santosh Mishra, a researcher in the Hoon laboratory. "When we exposed the Nppb-deficient mice to several itch-inducing substances, it was amazing to watch. Nothing happened. The mice wouldn't scratch." 

The researchers found that when Nppb or its nerve cell is not present, mice stopped scratching, as their bodies were not receiving the "itch" signal. Researchers also examined the area of the spine known as the dorsal horn, where the body's sensory signals are routed to the brain, and identified the protein Npra as being present.

"The receptors were exactly in the right place in the dorsal horn," said Hoon. "We went further and removed the Npra neurons from the spinal cord. We wanted to see if their removal would short-circuit the itch, and it did." 

Removing the receptor cells did not interfere with other sensations, such as temperature, pain and touch, so researchers concluded that "there is a dedicated signal to the brain that conveys the sensation of itch." Although then neurotransmitter known as GRP also plays a role in the itching sensation, the researchers said that it only becomes involved "after Nppb triggers the process". They also concluded that because the Nppb molecule is also used by the heart, kidneys and other vital parts of the body, attempting to control it through the neurotransmitter could have detrimental side effects.

"The larger scientific point remains," Hoon said. "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." 

In addition, research on animals does not always translate successfully on humans.