期刊
JOURNAL OF NEUROSCIENCE
卷 27, 期 42, 页码 11412-11415出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3600-07.2007
关键词
formaldehyde; TRPA1; TRP; thermoTRP; 4-HNE; pain; somatosensory
资金
- Korea Health Promotion Institute [A060341] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- NIDCR NIH HHS [DE016927, R01 DE016927] Funding Source: Medline
- NINDS NIH HHS [R01NS046303, R01 NS046303] Funding Source: Medline
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.
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