The roles of
ion channels in sensory neurons were examined in experimental models of
muscle pain in the rat. Rats were injected with 50 microl of 4%
carrageenan or subjected to an eccentric exercise (ECC) of the gastrocnemius muscle (GM). The Randall-Selitto and von Frey tests were performed on the calves to evaluate
mechanical hyperalgesia of the muscle. The changes in expression of four genes and
proteins of
ion channels in dorsal root ganglia were examined using quantitative PCR and immunohistochemistry, respectively. Effects of antagonists to transient receptor potential (TRP) channels and
acid sensing ion channels (ASICs) on the
mechanical hyperalgesia induced by
carrageenan injection or ECC were evaluated. The
mechanical hyperalgesia was observed 6-24h after
carrageenan injection and 1-3 days after ECC in the Randall-Selitto test. Infiltrations of the inflammatory cells in the GM were seen in
carrageenan-injected animals but not in those subjected to ECC. Expressions of genes and
proteins in sensory neurons showed no changes.
Intramuscular injection of antagonists to TRPV1 showed an almost complete suppressive effect on ECC-induced muscle
hyperalgesia but not a
carrageenan-induced one. Antagonists to TRP channels and ASICs showed suppressive effects for both
carrageenan- and ECC-induced muscle
hyperalgesia. The
carrageenan injection and ECC models are useful models of acute inflammatory
pain and delayed onset
muscle soreness (DOMS), respectively, and the time course and underlying etiology might be different. TRP channels and ASICs are closely related to the development of muscle
mechanical hyperalgesia, and TRPV1 is involved in ECC-induced DOMS.