 TRPA1 channels are expressed in nociceptive neurons and the mammalian cochlea, where their function is unknown. In the cochlea, TRPA1 activation in supporting Henson cells causes prolonged CA2 plus responses, which propagate across the organ of caulty and cause contraction of pillar and dytus cells. These contractions are mediated by CA2 plus dependent machinery, similar to that found in dytus cells. TRPA1 channels are activated by endogenous products of oxidative stress and extracellular ATP, which are present in vivo after acoustic trauma. This leads to support cell contractions, which can alter cochlea sensitivity. TRPA1 deficiency results in larger but less prolonged noise-induced temporary shifts of hearing thresholds, accompanied by permanent changes of latencies of auditory brainstem responses. Thus, TRPA1 channels contribute to the regulation of cochlea sensitivity after acoustic trauma. This article was authored by Catalina Valesortiga, Rubens Topanion, Stephanie E. Edelman, and others. We are article.tv, links in the description below.