Korean J Physiol Pharmacol.  2006 Dec;10(6):297-302.

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

• Shin HK
• Lee KH
• Cho CH

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 (30microgram/paw). Intrathecal or intraplantar pre-administration and intrathecal post-treatment 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 melittin-induced 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.

Keyword

Melittin; Nociceptive response; TMB-8; Quin 2

MeSH Terms

Animals
Bee Venoms
Calcium Channels
Calcium*
Chelating Agents
Hyperalgesia
Ions*
Melitten
Nociception*
Peripheral Nerves
Posterior Horn Cells
Prostaglandin-Endoperoxide Synthases
Rats*
Receptors, Glutamate
Receptors, Serotonin
Bee Venoms
Calcium
Calcium Channels
Chelating Agents
Ions
Melitten
Prostaglandin-Endoperoxide Synthases
Receptors, Glutamate
Receptors, Serotonin