Abstract
Previously we showed the existence of muscular mechanical hyperalgesia (DOMS) after lengthening contraction (LC) in rats. The mechanical withdrawal threshold of EDL muscle underwent LC decreased 1 day to 3 days after LC. It returned to the pre-LC value 4 days after LC (Taguchi et al, J. Physiol., 2005). In addition, we showed that administration of selective COX-2 inhibitors, Zaltoprofen and Celecoxib, before LC, but not after LC, blocked the development of the mechanical hyperalgesia elicited by LC. Meanwhile, it was reported that intramuscular injection of NGF induced lasting tenderness (Svennson et al, Pain, 2003). Therefore, we examined the expression of COX-2 and NGF mRNA in EDL muscle immediately after LC (0hr), 3, 6, 12 hrs and 1, 2, 3, 5 days after LC, and effects of anti-rat β NGF antibody on DOMS. EDL muscle without LC was used as a control. Expression of COX-2 mRNA increased 0-12 hrs and returned to the control value 1day after LC. Expression of COX-2 protein determined by western blotting also increased 0-12 hrs after LC. On the other hand, expression of NGF mRNA increased a little later, namely, 12 hrs-2 days after LC. To know if NGF is involved in DOMS, we examined effects of anti-rat β-NGF antibody (R&D systems). Rats were administered anti-NGF antibody (10 μg/ 5 μl, i. m.) or saline 6 hrs after LC under light halothane anesthesia. Anti-NGF completely blocked the development of the mechanical hyperalgesia. These results suggest that COX-2 acts as a trigger of the development of mechanical hyperalgesia and NGF was involved later in DOMS than COX-2. [J Physiol Sci. 2008;58 Suppl:S163]
