Area in the brain stem acts as a relay station between spinal cord and yet-unknown destination for prickly sensations
Scientists have traced the sensation of itch to a place you can’t scratch.
The discomfort of a mosquito bite or an allergic reaction activates itch-sensitive nerve cells in the spinal cord. Those neurons talk to a structure near the base of the brain called the parabrachial nucleus, researchers report in the Aug. 18 Science. It’s a region that’s known to receive information about other sensations, such as pain and taste.
The discovery gets researchers one step closer to finding out where itch signals ultimately end up. “The parabrachial nucleus is just the first relay center for [itch signals] going into the brain,” says study coauthor Yan-Gang Sun, a neuroscientist at the Chinese Academy of Sciences in Shanghai.
Understanding the way these signals are processed by the brain could someday provide relief for people with chronic itch, Sun says. While the temporary itchiness of a bug bite is annoying, longer term, “uncontrollable scratching behavior can cause serious skin damage.”
Previous studies have looked at the way an itch registers on the skin or how neurons convey those sensations to the spinal cord. But how those signals travel to the brain has been a trickier question, and this research is a “major step” toward answering it, says Zhou-Feng Chen, director of the Center for the Study of Itch at Washington University School of Medicine in St. Louis.
A network of neurons in the spinal cord wrangles itch signals, previous research suggests. In particular, spinal neurons that make a protein called gastrin-releasing peptide receptor have been shown to be important in itch signaling. But those neurons didn’t link up directly to the parabrachial nucleus, or PBN, Sun’s team found; instead, they talked to other neurons that send messages to the PBN.
When mice were given injections of a drug that induces allergic itching, the rodents showed greater activity in those neurons connecting the spinal cord to the PBN, Sun and colleagues found. In another experiment, the researchers made neurons going to the PBN light-sensitive, and then used light to stop those neurons from sending messages. When those nerve cells were blocked, mice given an itch-triggering drug scratched less.
It’s too soon to say whether itch signals in humans follow the same route — or whether all kinds of itches take the same path. An allergic itch is different from the sort of itch that comes from a light touch, and the two might be handled differently by the brain (SN: 11/22/08, p. 16). And mice, unlike humans, can’t actually describe how itchy they’re feeling. So scientists have to rely on clues like scratching, a reaction to an itch, not a direct measurement of the sensation itself. Which raises the question: If you don’t feel an urge to scratch an itch, is the itch really there at all?
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