期刊
MOLECULAR PAIN
卷 3, 期 -, 页码 -出版社
SAGE PUBLICATIONS INC
DOI: 10.1186/1744-8069-3-40
关键词
-
资金
- NIA NIH HHS [T32 AG023481] Funding Source: Medline
- NIDCR NIH HHS [DE016927, R01 DE016927] Funding Source: Medline
- NINDS NIH HHS [NS046303, R01 NS046303] Funding Source: Medline
Mechanical hyperalgesia is a clinically-relevant form of pain sensitization that develops through largely unknown mechanisms. TRPA1, a Transient Receptor Potential ion channel, is a sensor of pungent chemicals that may play a role in acute noxious mechanosensation and cold thermosensation. We have developed a specific small molecule TRPA1 inhibitor (AP18) that can reduce cinnameldehyde-induced nociception in vivo. Interestingly, AP18 is capable of reversing CFA-induced mechanical hyperalgesia in mice. Although TRPA1-deficient mice develop normal CFA-induced hyperalgeisa, AP18 is ineffective in the knockout mice, consistent with an on-target mechanism. Therefore, TRPA1 plays a role in sensitization of nociception, and that compensation in TRPA1-deficient mice masks this requirement.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据