Abstract
Melittin is the main toxin of bee venom. Previously, we have reported that intradermal injection of melittin into the volar aspect of forearm in humans produces a temporary pain and a subsequent sustained neurogenic-inflammation-skin temperature increase. Furthermore, not only subcutaneous melittin but also subcutaneous glutamate produced neurogenic inflammation on the rats' hindpaw. Aim of the present study was to confirm the involvement of NMDA receptors on melittin-induced neurogenic inflammation. We examined the neurogenic inflammation-skin temperature increase and glutamate release after melittin was injected subcutaneously into the hindpaw of pentobarbital-anesthetized rats. Skin temperature increase was analyzed using the computer-assisted-thermography. Subcutaneous glutamate was collected through a microdialysis probe, and glutamate level was measured using the HPLC-ECD method. Furthermore we examined the effect of NMDA receptor agonist and antagonist on the neurogenic inflammation-skin temperature increase. Intraplantar injection of melittin increased both skin temperature and glutamate level in subcutaneous microdialysate. Intraplantar injection of NMDA produced significant skin temperature increase compared with vehicle injection. Co-injection of MK-801 dose-dependently suppressed melittin-induced skin temperature increase. These findings suggest that melittin-induced neurogenic inflammation is enhanced through activation of peripheral NMDA receptors by peripherally released glutamate. [J Physiol Sci. 2008;58 Suppl:S163]
