Cold, dry winter weather can wreak havoc on our skin, drying it out and making us feel like one giant itch. Yet when it comes to scratching all of those dry patches, something inside our brains signals when it’s time to stop. That moment of relief is not accidental, and scientists have now pinpointed the key mechanisms behind it. The findings are being presented this weekend at the 70th Biophysical Society Annual Meeting in San Francisco, California.
Outside of winter, chronic itch affects millions of people with conditions including eczema, psoriasis, and kidney disease. Understanding the precise biological mechanisms that regulate itch—including what tells us to stop scratching before we get hurt—could help scientists develop better treatment.
In the new study, researchers from the University of Louvain in Brussels, Belgium, found an unexpected role in a specific ion channel. These channels in the body allow ions—atoms with an electrical charge—to flow in and out of the neuron’s membrane in response to a physical or chemical stimulus. These channels help the body’s nervous system detect temperature, pressure, and stress to various tissues.
The team specially found that the ion channel TRPV4 in mechanically evoked itch. TRPV4 is in a family of ion channels that function like molecular gates within sensory neurons. TRPV4 has long been suspected to participate in itch, but has not been well studied.
“We were initially studying TRPV4 in the context of pain,” Roberta Gualdani, a study co-author and molecular biologist, said in a statement. “But instead of a pain phenotype, what emerged very clearly was a disruption of itch, specifically, how scratching behavior is regulated.”
To probe the role that ion channels like TRPV4 play in the sensation to scratch, Gualdani’s team genetically engineered a mouse to serve as a model. They only deleted TRPV4 in the mouse’s sensory neurons, and not all of its tissues. This more neuron-specific approach helped them identify the channel was active.
They found that TRPV4 is expressed in neurons that are associated with touch and in some types of sensory neurons that are linked to itch and pain pathways.
The team then induced a chronic itch condition resembling atopic dermatitis—a common chronic condition that causes dry skin. The mice without TRPV4 in their neurons scratched less frequently, but each round of scratching lasted much longer than normal.
“At first glance, that seems paradoxical,” Gualdani said. “But it actually reveals something very important about how itch is regulated.”
According to the team, their findings suggest that TRPV4 does not simply generate itch. Instead, it helps trigger a negative feedback signal in sensory neurons that tells the spinal cord and brain that the scratching has been enough and it’s time to stop. Without this signal, that feeling of relief is muted, and excessive scratching continues. In other words, TRPV4 is part of the nervous system’s internal “stop-scratching” signal.
“When we scratch an itch, at some point we stop because there’s a negative feedback signal that tells us we’re satisfied,” Gualdani explained. “Without TRPV4, the mice don’t feel this feedback, so they continue scratching much longer than normal.”
While broadly blocking TRPV4 may not be a solution to chronic itch, it’s a start towards creating new treatments.
“Future therapies may need to be much more targeted—perhaps acting only in the skin, without interfering with the neuronal mechanisms that tell us when to stop scratching,” said Gualdani.
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