Abstract
Aim of Investigation: 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 glutamate receptors on melittin-induced neurogenic inflammation. Methods: Melittin or glutamate was injected subcutaneously into the hindpaw of pentobarbital-anesthetized rats. NMDA receptor antagonist, MK-801 or AMPA receptor antagonist, CNQX was injected simultaneously with melittin/glutamate. Peripheral glutamate was collected by microdialysis and quantified using HPLC. Skin temperature increase was analyzed using the computer-assisted-thermography for the evaluation of neurogenic inflammation. Results: Microdialysate concentrations of glutamate were increased significantly following subcutaneous melittin injection. Simultaneous MK-801 injection suppressed not only glutamate-induce-neurogenic inflammation but also melittin-induce-neurogenic inflammation. The suppression effects of CNQX were weak. Conclusion: These data demonstrated that glutamate released following melittin injection partially contributed to neurogenic inflammation by activating NMDA receptors on nociceptors. Melittin-induced glutamate release suggested to prolong the melittin-induced neurogenic inflammation. [J Physiol Sci. 2006;56 Suppl:S179]
