TRPA1 contributed to the neuropathic pain induced by docetaxel treatment. (31st March 2017)

• Record Type: Journal Article
• Authors: Huang, Kun; Bian, Donglin; Jiang, Bin; Zhai, Qixi; Gao, Ningning; Wang, Ruiying
• Is Part Of: Cell biochemistry and function. Volume 35:Number 3(2017)
• Page Start: 141
• Page End: 143
• Publication Date: 2017-03-31
• Subjects: docetaxel -- mechanical allodynia -- pain -- TRPA1; Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3258
• Languages: English
• ISSNs: 0263-6484

Abstract

Abstract : Peripheral mechanical neuropathic pain is a serious side effect of docetaxel chemotherapy for cancer. However, the underlying mechanism for this side effect is unknown. In the present study, we found that docetaxel treatment induced mechanical allodynia in rats. We further revealed that the transient receptor potential ankyrin subtype 1 protein (TRPA1) protein level is upregulated and the TRPA1 activator allyl isothiocyanate induced larger ion currents in the dorsal root ganglion neurons from the docetaxel treated rats. In addition, application the TRPA1 blocker Ap18 reversed the docetaxel‐induced mechanical hypersensitivity. We suggest that the docetaxel‐induced mechanical allodynia is mediated by upregulation of TRPA1 in dorsal root ganglion neurons.