Here's the theory: When we scratch an itch, it causes a small amount of pain to the affected skin. That pain serves as a distraction, numbing us to the itch itself.
But the pain also triggers the release of serotonin in the brain. Serotonin dulls pain, but it also reacts with neurons that carry itch signals to the brain. So as the pain of the scratch dies away, the itch roars back even stronger. That causes the itching-scratching cycle that leaves us with raw, itchy skin.
"The problem is that when the brain gets those pain signals, it responds by producing the neurotransmitter serotonin to help control that pain," lead author Zhou-Feng Chen, the director of Washington University's Center for the Study of Itch, said in a statement. "But as serotonin spreads from the brain into the spinal cord, we found the chemical can 'jump the tracks,' moving from pain-sensing neurons to nerve cells that influence itch intensity."
The study used mice, but Chen believes the findings apply to humans as well. In the study, Chen and his colleagues bred mice that couldn't produce serotonin. When they were injected with something that should have made them itch, they scratched less than mice who were able to make normal amounts of serotonin.
But unfortunately, it wouldn't be practical for humans to treat itch by blocking serotonin. It's a pretty important chemical -- one involved in everything from growth to mood regulation. But Chen did have some luck with interrupting the itch-related nerve cells that react to serotonin, so it's possible that their work could lead to more productive scratching in the future.