An ion channel essential for sensing chemical damage

Lindsey J. Macpherson, Bailong Xiao, Kelvin Y. Kwan, Matt J. Petrus, Adrienne E. Dubin, Sun Wook Hwang, Benjamin Cravatt, David P. Corey, Ardem Patapoutian

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219 Citations (Scopus)

Abstract

Tissue damage and its downstream consequences are experimentally assayed by formaldehyde application, which indiscriminately modifies proteins and is presumed to cause pain through broadly acting mechanisms. Here we show that formaldehyde activates the ion channel TRPA1 and that TRPA1-deficient mice exhibit dramatically reduced formaldehyde-induced pain responses. 4-Hydroxynonenal, a reactive chemical produced endogenously during oxidative stress, and other related aldehydes also activate TRPA1 in vitro. Furthermore, painful responses to iodoacetamide, a nonspecific cysteine-alkylating compound, are abolished in TRPA1-deficient mice. Therefore, although these reactive chemicals modify many proteins, the associated pain appears mainly dependent on a single ion channel.

Original languageEnglish
Pages (from-to)11412-11415
Number of pages4
JournalJournal of Neuroscience
Volume27
Issue number42
DOIs
Publication statusPublished - 2007 Oct 17

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Keywords

  • 4-HNE
  • Formaldehyde
  • Pain
  • Somatosensory
  • ThermoTRP
  • TRP
  • TRPA1

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Macpherson, L. J., Xiao, B., Kwan, K. Y., Petrus, M. J., Dubin, A. E., Hwang, S. W., Cravatt, B., Corey, D. P., & Patapoutian, A. (2007). An ion channel essential for sensing chemical damage. Journal of Neuroscience, 27(42), 11412-11415. https://doi.org/10.1523/JNEUROSCI.3600-07.2007