There’s itch, and then there’s itch.
Research led by Clifford Woolf, an HMS professor of neurology, and David Roberson, an HMS graduate student in neuroscience, has revealed distinct sets of itch-generating neurons that explain why itch therapies often fail, and suggests ways to selectively silence itch.
“We think this has therapeutic implications,” says Woolf, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital.
One day, the sensation that sends your fingernails scrambling over your scalp may open the door to relief. Building on science that uses the heat from chili peppers to unlatch the cellular gates to admit a painkiller, the researchers have shown in mice that a lidocaine-like drug can enter the nerve cells that spark itch and squelch the sensation.
Antihistamines don’t always work on itch because most itch is not caused by histamine, the substance that induces hives and other miseries. Eczema, atopic dermatitis, and dry-skin itches are spurred by other irritants, prompting specific nerve cells to send signals from skin to spinal cord that scream, “Scratch!”
In their paper in the May online issue of Nature Neuroscience, Woolf and Roberson show for the first time that different nerve fibers sense different kinds of itch.
Woolf came to study itch by way of landmark work on pain that he and others, including Bruce Bean, the Robert Winthrop Professor of Neurobiology at HMS, published in 2007 in Nature. The scientists delivered the lidocaine derivative QX-314 into pain-sensing nerve fibers via large pores, called ion channels, in nerve-cell membranes. Capsaicin, the searing component in chili peppers, opened an ion channel that allowed QX-314 to selectively enter pain-sensing neurons.
Roberson is testing topical QX-314 creams in mice.
“We are excited about the possibility that this discovery could one day provide long-lasting relief to people suffering from chronic itch,” Roberson says.