抄録
It is well known that capsaicin application to the facial skin causes a decrease in pain threshold in humans. We also observed that the application of capsaicin to the monkey face causes a decrease in cold detection threshold. However, the neural mechanisms of the change in cold pain threshold following capsaicin treatment are still remained unclear. The aim of present study is to clarify the neural mechanisms underlying capsaicin-induced cold allodynia in face. The phosphorylation of the extracellular signal-regulated protein kinase (ERK) was precisely analyzed in the trigeminal spinal subnucleus caudalis (Vc) neurons in pentobarbital anesthetized rats (sodium pentobarbital: 50mg/kg, ip.) after the topical application of capsaicin (10mM) to the facial skin. A large number of pERK-LI cells was observed in the superficial laminae of Vc after heat stimulation of the face in vehicle treated rats, but not after cold stimulation. However, the number of pERK-LI cells was significantly increased after cold stimulation of the face in the rats with capsaicin treatment compared with vehicle treated rats as well as heat stimulation. The present findings suggest that the sensitization of TRPV1 channels is involved in capsaicin-induced cold allodynia in the facial skin. [J Physiol Sci. 2008;58 Suppl:S164]
