Acid-sensing ion channel 3 expression is increased in dorsal root ganglion, hippocampus and hypothalamus in remifentanil-induced hyperalgesia in rats

Abstract

BackgroundRemifentanil induces hyperalgesia, but the underlying mechanisms are not fully understood. Acid-sensing ion channel 3 (ASIC3) plays a regulatory role in the pain pathway. This study aimed to explore the effect of remifentanil administration on postoperative pain and on ASIC3 expression at the prespinal and supraspinal levels in a rat model. MethodsRats were randomly allocated to the control, incision, remifentanil, and remifentanil + incision groups. Remifentanil was given by a 1-h intravenous infusion prior to plantar incision. Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured at different time points before and after incision to evaluate mechanical and thermal hyperalgesia, respectively. The dorsal root ganglion (DRG), hippocampus, and hypothalamus were obtained after sacrifice at 48 h post-incision for determination of the protein expression of ASIC3 using western blot. ResultsRemifentanil administration significantly induced mechanical and thermal hyperalgesia from 2 to 48 h after incision. In addition, remifentanil exposure remarkably stimulated ASIC3 protein expression in DRG, hippocampus, and hypothalamus of rats at 48 h after incision. ConclusionRemifentanil-induced hyperalgesia is accompanied by increased ASIC3 expression at the DRG and supraspinal levels, implying a possible involvement of ASIC3 in remifentanil-induced hyperalgesia.