Scientists Found the Itch Molecule—and They Know How to Turn it Off

It is not the louse we hate. Nor is it the mosquito, shirt tag, wool sweater, chicken pock, or sudden rash that torments us—the itching itself is what drives us mad. But finally, scientists have been able to identify the molecule that signals our brain to start scratching us raw—and removing it kills itchiness forever. But don't we itch for a reason?


The molecular geneticists in question, Santosh Mishra and Mark Hoon of the National Institutes of Health, began by examining the neurotransmitter chemicals in our spinal column that pass along sensory information such as heat, pain, and yes, itchiness. What they noticed was that, when mice were exposed to a variety of itch-inducing triggers, one particular chemical began releasing in excess: natriuretic polypeptide b (Nppb).

The true test came when the pair created genetically engineered mice that couldn't produce the Nppb transmitter. First they tested to see if the super-mice were still able to feel other sensations such as heat and pain, to which they all responded normally. So the removal didn't affect their response to other stimuli. Then, out came the itch-triggers (such as histamine) again. While the normal mice immediately started scratching themselves raw, the engineered mice remained calm and undoubtedly itch free. According to Mishra:

It was amazing to watch. Nothing happened. The mice wouldn’t scratch.
Until the scientists re-injected them with Nppb, that is, at which point all bets were off and their claws went to town.

Next, they were able to identify a specific type of neuron in the mice's spines with receptors called natriuretic peptide receptor A (Npra), which seemed like a likely candidate to accept Nppb. And sure enough, once the Npra was removed from normal mice, they appeared totally impervious to any itching whatsoever. What's more, they were still able to feel other sensations, so lacking this neuron wouldn't affect their sense of pain or touch.

And even though these tests were performed on mice instead of humans, we share incredibly similar nervous systems with our more rodent-oriented friends. So at the very least, this gives us a far greater understanding of our own itch reflex. But it could also very likely lead to solutions for people who produce an excess of Nppb and help make stronger, more effective itch treatments—or perhaps even total cures.

It's not going to be totally smooth sailing, though. Nppb is significant not just for the sensory nuisance it causes but also for its ability to help regulate blood circulation and pressure. Which means shutting it off entirely might present a bit of a problem. In general, there's still a lot that we don't understand about itching and its evolutionary benefits, but our potential newfound ability to turn it on and off is certainly an incredible first step.