If you get an itch, you probably scratch it. Even reading about itchiness right now might make you want to scratch something.
Why does scratching the area where an itch pops up generally make the sensation go away? Scientists recently uncovered more about what exactly is going on with scratching.
“When we scratch an itch, at some point we stop because there’s a negative feedback signal that tells us we’re satisfied,” explained Roberta Gualdani, professor at the University of Louvain in Brussels.
This feedback signal is linked to ion channel TRPV4. It is a channel that has been shown to mediate and regulate certain processes in the body. TRPV4 also appears to be mechanosensitive, meaning that it has as specific response to mechanical stimulation.
“TRPV4 belongs to a family of ion channels that act as molecular gates in the membranes of sensory neurons, allowing ions to flow in response to physical or chemical stimuli,” according to a press release from the Biophysical Society. “These channels help the nervous system detect temperature, pressure, and tissue stress. While TRPV4 has long been suspected to participate in mechanosensation, its role in itch, and especially in chronic itch, has remained controversial.”
Gualdani and her team were studying TRP4 in the context of pain. However, she said they found that they instead found “what emerged very clearly was a disruption of itch,” and “specifically, how scratching behavior is regulated.”
To study this further, Gualdani’s team engineered a genetic mouse model with selectively deleted TRP4 in sensory neurons. They demonstrated that TRP4 is expressed in neurons “classically associated with touch” and other neurons linked to itch.
Then, the researchers induced a condition similar to atopic dermatitis in the engineered mice. Per the press release, the results were “striking.”
Mice that didn’t have the neuronal TRPV4 didn’t scratch as often as the other mice. Yet, whenever they did scratch, they scratched for longer amounts of time.
Overall, the team found that TRP4 both generates itch and triggers the feedback signal that tells the body scratching has worked. Without it, mice went on scratching for longer than normal because the relief sensation is blunted.
“At first glance, that seems paradoxical,” Gualdani said. “But it actually reveals something very important about how itch is regulated.”
Interestingly, research about scratching published last year found that “mice able to scratch experienced more inflammation and a stronger immune response, but were less likely to harbor Staphylococcus aureus, a harmful bacterium known to cause skin infections, compared with the mice that couldn’t scratch.”
Research results from Gualdani’s team also indicate that TRP4’s role in itch is more complicated than previously thought. Its apparent dual role in the itching sensation and relief has implications for drug development in the future.
“Chronic itch affects millions of people with conditions like eczema, psoriasis, and kidney disease, yet effective treatments remain limited,” the Biophysical Society noted. “Understanding the precise mechanisms that regulate itch – including when to stop scratching – could open new avenues for therapeutic development.”
Gualdani’s team presented their research during the 70th Biophysical Society Annual Meeting in San Francisco from, being held this Saturday through next Tuesday. Other research presented at the event also explored why cold temperatures and exposure to menthol generate similar sensations – that’s linked to another channel called TRPM8.