HTR7 Mediates Serotonergic Acute and Chronic Itch.

Autor:	Morita T; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720, USA., McClain SP; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA., Batia LM; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA., Pellegrino M; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA., Wilson SR; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720, USA., Kienzler MA; Neurobiology Course, Marine Biological Laboratory, Woods Hole, MA 02543, USA., Lyman K; Neurobiology Course, Marine Biological Laboratory, Woods Hole, MA 02543, USA., Olsen AS; Neurobiology Course, Marine Biological Laboratory, Woods Hole, MA 02543, USA., Wong JF; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA., Stucky CL; Departments of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, WI 53226, USA., Brem RB; Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: rbrem@buckinstitute.org., Bautista DM; Department of Molecular & Cell Biology, 142 Life Sciences Addition, University of California, Berkeley, Berkeley, CA 94720-3200, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: dbautista@berkeley.edu.
Jazyk:	angličtina
Zdroj:	Neuron [Neuron] 2015 Jul 01; Vol. 87 (1), pp. 124-38. Date of Electronic Publication: 2015 Jun 11.
DOI:	10.1016/j.neuron.2015.05.044
Abstrakt:	Chronic itch is a prevalent and debilitating condition for which few effective therapies are available. We harnessed the natural variation across genetically distinct mouse strains to identify transcripts co-regulated with itch behavior. This survey led to the discovery of the serotonin receptor HTR7 as a key mediator of serotonergic itch. Activation of HTR7 promoted opening of the ion channel TRPA1, which in turn triggered itch behaviors. In addition, acute itch triggered by serotonin or a selective serotonin reuptake inhibitor required both HTR7 and TRPA1. Aberrant serotonin signaling has long been linked to a variety of human chronic itch conditions, including atopic dermatitis. In a mouse model of atopic dermatitis, mice lacking HTR7 or TRPA1 displayed reduced scratching and skin lesion severity. These data highlight a role for HTR7 in acute and chronic itch and suggest that HTR7 antagonists may be useful for treating a variety of pathological itch conditions. (Copyright © 2015 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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