PT - JOURNAL ARTICLE AU - Sarah R. Wilson AU - Aislyn M. Nelson AU - Lyn Batia AU - Takeshi Morita AU - Daniel Estandian AU - David M. Owens AU - Ellen A. Lumpkin AU - Diana M. Bautista TI - The Ion Channel TRPA1 Is Required for Chronic Itch AID - 10.1523/JNEUROSCI.5318-12.2013 DP - 2013 May 29 TA - The Journal of Neuroscience PG - 9283--9294 VI - 33 IP - 22 4099 - http://www.jneurosci.org/content/33/22/9283.short 4100 - http://www.jneurosci.org/content/33/22/9283.full SO - J. Neurosci.2013 May 29; 33 AB - 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.