Cutaneous C-polymodal fibers lacking TRPV1 are sensitized to heat following inflammation but fail to drive heat hyperalgesia in the absence of TPV1 containing C-heat fibers

摘要

BackgroundPrevious studies have shown that the TRPV1 ion channel plays a critical role in the development of heat hyperalgesia after inflammation, as inflamed TRPV1-/- mice develop mechanical allodynia but fail to develop thermal hyperalgesia. In order to further investigate the role of TRPV1, we have used an ex vivo skinerve/DRG preparation to examine the effects of CFA-induced-inflammation on the response properties of TRPV1-positive and TRPV1-negative cutaneous nociceptors.