期刊
JOURNAL OF NEUROSCIENCE
卷 33, 期 22, 页码 9283-9294出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5318-12.2013
关键词
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资金
- National Institute of Arthritis and Musculoskeletal and Skin Diseases-National Institutes of Health [R01 AR051219, R01 AR059385]
- McNair Scholars Program
- National Science Foundation
- Columbia University Skin Disease Research Center Tissue Culture and Histology Core and Advanced Imaging Core
- National Institutes of Health Grant [P30AR044535, P30CA013696]
- Herbert Irving Comprehensive Cancer Center Confocal and Specialized Microscopy Shared Resource
Chronic itch is a debilitating condition that affects one in 10 people. Little is known about the molecules that mediate chronic itch in primary sensory neurons and skin. We demonstrate that the ion channel TRPA1 is required for chronic itch. Using a mouse model of chronic itch, we show that scratching evoked by impaired skin barrier is abolished in TRPA1-deficient animals. This model recapitulates many of the pathophysiological hallmarks of chronic itch that are observed in prevalent human diseases such as atopic dermatitis and psoriasis, including robust scratching, extensive epidermal hyperplasia, and dramatic changes in gene expression in sensory neurons and skin. Remarkably, TRPA1 is required for both transduction of chronic itch signals to the CNS and for the dramatic skin changes triggered by dry-skin-evoked itch and scratching. These data suggest that TRPA1 regulates both itch transduction and pathophysiological changes in the skin that promote chronic itch.
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