Abstract
In the present study, the activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) in the rostral ventromedial medulla (RVM) following the injection of complete Freund's adjuvant (CFA) into the rat hindpaw was examined in order to clarify the mechanisms underlying the dynamic changes in the descending pain modulatory system after peripheral inflammation. Phospho-ERK-immunoreactive (p-ERK-IR) and phospho-p38 MAPK-immunoreactive (p-p38 MAPK-IR) neurons were observed in the nucleus raphe magnus (NRM) and nucleus reticularis gigantocellularis pars alpha (GiA). Inflammation induced the activation of ERK in the RVM, with a peak at 7 hours after the injection of CFA into the hindpaw and a duration of 24 hours. In the RVM, the number of p-ERK-IR neurons per section in rats killed at 7 hours after CFA injection (14.2±1.7) was significantly higher than that in the control group (4.5±0.9) (p<0.01). In contrast, activation of p38 MAPK in the RVM was observed within 1 hour after CFA injection. After CFA injection, about 60% of p-ERK-IR neurons, about 40% of p-p38 MAPK-IR neurons in the RVM were serotonergic neurons. The p-ERK-positive rate of RVM serotonergic neurons in the rats with inflammation was seven times higher than that in control rats (p<0.01). These findings suggest that inflammation-induced-activation of ERK and p38 MAPK in the RVM may be involved in the plasticity in the descending pain modulatory system following inflammation. [J Physiol Sci. 2007;57 Suppl:S113]
