<b>Melittin-induced neurogenic inflammation is increased through activation of peripheral glutamate receptors</b>

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  • Koyama Natsu
    Department of Physiology, Shiga University of Medical Science
  • Iwashita Narihito
    Department of Physiology, Shiga University of Medical Science Department of Anesthesiology, Shiga University of Medical Science

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  • メリチンによる神経性炎症は末梢グルタミン酸受容体を介する

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Abstract

   Melittin is the main toxin of bee venom. Previously, we have reported that intradermal injection of melittin into the 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 peripheral glutamate receptors on melittininduced neurogenic inflammation.<br>   Melittin was injected subcutaneously into the hindpaw of pentobarbital-anesthetized rats. Cutaneous glutamate was collected by microdialysis probe and measured using the HPLC-ECD method. Subcutaneous melittin injection caused significantly increase in microdialysate levels of glutamate in the skin, the NMDA receptor antagonist MK-801 or the non-NMDA receptor antagonist CNQX was injected simultaneously with melittin. Skin temperature increase was analyzed using the computer-assisted-thermography for the evaluation of neurogenic inflammation. Not only simultaneous MK-801 but also CNQX injection partially suppressed melittin-induce-neurogenic inflammation. These data suggest that NMDA ⁄ non-NMDA receptors on nociceptors are involved in the melittin-induced neurogenic inflammation.

Journal

  • PAIN RESEARCH

    PAIN RESEARCH 22 (1), 35-41, 2007

    JAPANESE ASSOCIATION FOR STUDY OF PAIN

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