Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Apr 18;12:1287–1296. doi: 10.2147/JPR.S197168

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 Cao et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

Schematic presentation of the mechanisms of TRPM8 blockade on cold hyperalgesia in the dorsal root ganglions of chronic constriction injury (CCI) rats. CCI increases expression of TRPM8, PKC, p-PKC and NF-κB p65 in the ipsilateral DRGs of CCI rats. Intrathecal injection of AMTB blocks TRPM8, and offset these effects induced by CCI. NF-κB inhibitor PDTC enhances AMTB’s anti-cold pain effect. These suggest that TRPM8 channels in DRGs participate in the pathogenesis of cold hyperalgesia in rats with neuropathic pain, which could be regulated by PKC and NF-κB signaling. Arrowheads=activate, short bars=inhibition.