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Calcium Ions are Involved in Modulation of Melittin-induced Nociception in Rat: II. Effect of Calcium Chelator  

Shin, Hong-Kee (Department of Physiology, College of Medicine, Hanyang University)
Lee, Kyung-Hee (Department of Physiology, College of Medicine, Hanyang University)
Cho, Chul-Hyun (Department of Orthopedic Surgery, School of Medicine Keimyung University)
Publication Information
The Korean Journal of Physiology and Pharmacology / v.10, no.6, 2006 , pp. 297-302 More about this Journal
Abstract
Melittin, a major component of bee venom, produces a sustained decrease in mechanical threshold, and an increase in spontaneous flinchings and paw thickness, which are characteristics similar to those induced by whole bee venom. Melittin-induced nociception has been known to be modulated by the changes in the activity of excitatory amino acid receptors, voltage-dependent calcium channels, cyclooxygenase and serotonin receptors. The present study was undertaken to investigate the role of calcium chelators (TMB-8 & Quin 2) in melittin-induced nociceptive responses. Changes of mechanical threshold and spontaneous flinching behaviors were measured at a given time point following intraplantar injection of melittin ($30{\mu}g/paw$). Intrathecal or intraplantar pre-administration and intrathecal posttreatment of TMB-8 and Quin 2 significantly prevented the melittin-induced reduction of mechanical threshold, and intraplantar or intrathecal pre-treatment of TMB-8 and Quin 2 suppressed melittininduced flinching behaviors. These results indicate that calcium ion in the spinal dorsal horn neurons and peripheral nerves plays an important role in the production and maintenance of mechanical allodynia and spontaneous pain by melittin.
Keywords
Melittin; Nociceptive response; TMB-8; Quin 2;
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