| First Author | del Camino D | Year | 2010 |
| Journal | J Neurosci | Volume | 30 |
| Issue | 45 | Pages | 15165-74 |
| PubMed ID | 21068322 | Mgi Jnum | J:166452 |
| Mgi Id | MGI:4845796 | Doi | 10.1523/JNEUROSCI.2580-10.2010 |
| Citation | del Camino D, et al. (2010) TRPA1 contributes to cold hypersensitivity. J Neurosci 30(45):15165-74 |
| abstractText | TRPA1 is a nonselective cation channel expressed by nociceptors. Although it is widely accepted that TRPA1 serves as a broad irritancy receptor for a variety of reactive chemicals, its role in cold sensation remains controversial. Here, we demonstrate that mild cooling markedly increases agonist-evoked rat TRPA1 currents. In the absence of an agonist, even noxious cold only increases current amplitude slightly. These results suggest that TRPA1 is a key mediator of cold hypersensitivity in pathological conditions in which reactive oxygen species and proinflammatory activators of the channel are present, but likely plays a comparatively minor role in acute cold sensation. Supporting this, cold hypersensitivity can be induced in wild-type but not Trpa1(-/-) mice by subcutaneous administration of a TRPA1 agonist. Furthermore, the selective TRPA1 antagonist HC-030031 [2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl )acetamide] reduces cold hypersensitivity in rodent models of inflammatory and neuropathic pain. |
