The sensation of itching is hardwired into the nervous system and can be traced back to a small molecule released in the spinal cord, according to a new study in mice.
Researchers say this molecule, known as natriuretic polypeptide b (Nppb), triggers a signal that passes through the central nervous system. Ultimately, this signal is experienced as an itch. Since the nervous systems of humans and mice are similar, the researchers concluded that a similar process probably occurs in people.
"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.
The findings might someday help scientists develop treatments for chronic itch conditions, such eczema and psoriasis, the researchers suggested.
For the new study, the researchers first identified the signaling components on nerve cells that contain a molecule called TRPV1. These nerve cells help to monitor certain external conditions, such as extreme temperature changes or detecting pain. In examining how these cells recognize various sensations, the study authors screened the molecule, Nppb.
"We tested Nppb for its possible role in various sensations without success," study lead author Santosh Mishra, a researcher in the Hoon laboratory, said in the news release.
However, he added, "When we exposed the Nppb-deficient mice to several itch-inducing substances, it was amazing to watch. Nothing happened. The mice wouldn't scratch."
When Nppb or its nerve cell was not present, mice stopped scratching because the signal wasn't going through, the researchers explained.
The investigators also focused on the dorsal horn, an area of the spine where sensory signals from the body are routed to the brain in order to look for cells that receive incoming Nppb molecules. They identified the receptor as the protein Npra.
"The receptors were exactly in the right place in the dorsal horn," noted 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."
Because removing the receptor nerve cells did not affect other sensations -- such as temperature, pain and touch -- the researchers concluded there is a dedicated signal to the brain that conveys the sensation of itch. Although another neurotransmitter called GRP also plays a role in the sensation of itch, they pointed out that it becomes involved only after Nppb triggers the process.
However, since the Nppb molecule is also used by the heart, kidneys and other parts of the body, the researchers concluded that attempting to control itch through the neurotransmitter in the spine could have negative 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."
Research in animals often doesn't translate into success in human studies.
The study appeared online May 23 in the journal Science.