| First Author | Morita T | Year | 2015 |
| Journal | Neuron | Volume | 87 |
| Issue | 1 | Pages | 124-38 |
| PubMed ID | 26074006 | Mgi Jnum | J:227435 |
| Mgi Id | MGI:5700463 | Doi | 10.1016/j.neuron.2015.05.044 |
| Citation | Morita T, et al. (2015) HTR7 Mediates Serotonergic Acute and Chronic Itch. Neuron 87(1):124-38 |
| abstractText | 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. |
