An ion channel critical for some forms of itch is identified in a paper published online this week in Nature Neuroscience.
Itch, like pain, serves a protective function under normal conditions; however, chronic, pathological itch is a debilitating condition that accompanies numerous skin and systemic disorders. In many cases, pathological itch is resistant to antihistamine treatments.
Diana Bautista and colleagues used a host of pharmacological and genetic techniques to probe the pathways of histamine-independent itch in mice. They report that two chemicals that elicit histamine-independent itch ― including the antimalarial drug chloroquine, which can produce itching as an adverse side effect ― control neuronal excitability via an ion channel called TRPA1. Sensory neurons of mice deficient in TRPA1 have a substantially diminished response to chloroquine and the team found that the mice show little to no scratching in response to the drug.
These findings in mice may provide insight into pathological histamine-independent itch in humans.