HTR7 Mediates Serotonergic Acute and Chronic Itch. Neuron 2015 Jul 01;87(1):124-38
Date
06/16/2015Pubmed ID
26074006Pubmed Central ID
PMC4536073DOI
10.1016/j.neuron.2015.05.044Scopus ID
2-s2.0-84937516283 (requires institutional sign-in at Scopus site) 154 CitationsAbstract
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.
Author List
Morita T, McClain SP, Batia LM, Pellegrino M, Wilson SR, Kienzler MA, Lyman K, Olsen AS, Wong JF, Stucky CL, Brem RB, Bautista DMAuthor
Cheryl L. Stucky PhD Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Acute DiseaseAnimals
Chronic Disease
Dermatitis, Atopic
Disease Models, Animal
Ganglia, Spinal
Gene Expression Profiling
Humans
Mice
Mice, Inbred C57BL
Mice, Inbred DBA
Pruritus
RNA, Messenger
Receptors, Serotonin
Reverse Transcriptase Polymerase Chain Reaction
Serotonin
Serotonin Receptor Agonists
TRPA1 Cation Channel
Transient Receptor Potential Channels
