Feb 22, 2026
3 min read
Understanding how this signal works may lead to better treatments for chronic itching.
Cold, dry winter air can wreak havoc on our skin, drying it out and leaving us feeling like a giant itch.But when it comes to scratching all those dry patches, something in our brain signals that it's time to stop.This moment of relief is no coincidence, and scientists have now identified the underlying mechanisms behind it.The findings will be presented this weekend at the 70th Annual Meeting of the Biophysical Society in San Francisco, California.
Outside of winter, chronic itching affects millions of people with conditions such as eczema, psoriasis and kidney disease.Understanding the exact biological mechanisms that control itching -- including what tells us to stop scratching before we get hurt -- could help scientists develop better treatments.
In the new study, researchers from the University of Louvain in Brussels, Belgium, found an unexpected role for a specific ion channel.These body channels allow ions (electrically charged atoms) to flow in and out of the neuron membrane in response to a physical or chemical stimulus.These channels help the body's nervous system sense temperature, pressure, and stress in various tissues.
Specifically, the team found that the ion channel TRPV4 is involved in mechanically induced itch.TRPV4 belongs to a family of ion channels that act as molecular gates in sensory neurons.TRPV4 has long been suspected to be involved in itch, but has not been well studied.
"We initially studied TRPV4 in the context of pain," said co-author and molecular biologist Roberta Gualdani in a statement."But rather than a pain phenotype, what clearly emerged was a disruption in itch, specifically how scratching behavior is regulated."
To investigate the role of ion channels such as TRPV4 in patterning, Gualdani's group developed a mouse as a model.They deleted TRPV4 only in the mouse's sensory neurons, not in all its tissues.This more specific way of the neuron helped them understand that the channel was active.
They found that TRPV4 is expressed in neurons associated with touch, as well as certain sensory neurons associated with itch and pain pathways.
The team developed a type of atopic dermatitis - a disease that causes dry skin.Mice without TRPV4 in their neurons scratch more, but each stroke lasts longer than normal.
"At first glance, this seems paradoxical," Gualdani said."But it actually reveals something very important about how rash is regulated."
According to the team, their findings show that TRPV4 doesn't just cause itch.Instead, it helps trigger a negative feedback signal in sensory neurons that tells the brain and spinal cord that enough scratching is enough and it's time to stop.Without this signal, this feeling of comfort is interrupted and excessive itching continues.In other words, TRPV4 is part of the system's internal "stop itching" signal.is a nerve.
"When we scratch, we pause for a moment because there's a negative feedback signal that tells us we're satisfied," Cavaldani explained."Without TRPV4, mice don't feel that response, so they keep scratching longer than normal."
Although blocking TRPV4 in general is not a solution to chronic itch, it is the beginning of a new treatment.
“Future treatments may require more targeted treatments that can act only on the skin without interfering with the neural mechanisms that tell it when to stop scratching,” Gualdani said.
