Calcium Ions are Involved in Modulation of Melittin-induced Nociception in Rat: I. Effect of Voltage-gated Calcium Channel Antagonist.
- Author:
Hong Kee SHIN
1
;
Kyung Hee LE
Author Information
1. Department of Physiology, College of Medicine, Hanyang University, Seoul 133-791, Korea. shinhg@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Melittin;
Hyperalgesia;
Spontaneous pain;
Voltage-gated calcium channel antagonist
- MeSH:
Animals;
Calcium Channels*;
Calcium Channels, L-Type;
Calcium Channels, N-Type;
Calcium Channels, P-Type;
Calcium*;
Hyperalgesia;
Ions*;
Melitten;
Nociception*;
omega-Agatoxin IVA;
omega-Conotoxin GVIA;
Prostaglandin-Endoperoxide Synthases;
Protein Kinase C;
Rats*;
Receptors, Glutamate;
Serotonin;
Verapamil
- From:The Korean Journal of Physiology and Pharmacology
2006;10(5):255-261
- CountryRepublic of Korea
- Language:English
-
Abstract:
Melittin-induced nociceptive responses are mediated by selective activation of capsaicin-sensitive primary afferent fibers and are modulated by excitatory amino acid receptor, cyclooxygenase, protein kinase C and serotonin receptor. The present study was undertaken to investigate the peripheral and spinal actions of voltage-gated calcium channel antagonists on melittin-induced nociceptive responses. Changes in mechanical threshold and number of flinchings were measured after intraplantar (i.pl.) injection of melittin (30microg/paw) into mid-plantar area of hindpaw. L-type calcium channel antagonists, verapamil [intrathecal (i.t.), 6 or 12microg; i.pl.,100 & 200microg; i.p., 10 or 30 mg], N-type calcium channel blocker, omega-conotoxin GVIA (i.t., 0.1 or 0.5microg; i.pl., 5microg) and P-type calcium channel antagonist, omega-agatoxin IVA (i.t., 0.5microg; i.pl., 5microg) were administered 20 min before or 60 min after i.pl. injection of melittin. Intraplantar pre-treatment and i.t. pre- or post-treatment of verapamil and omega-conotoxin GVIA dose-dependently attenuated the reduction of mechanical threshold, and melittin-induced flinchings were inhibited by i.pl. or i.t. pre-treatment of both antagonists. P-type calcium channel blocker, omega-agatoxin IVA, had significant inhibitory action on flinching behaviors, but had a limited effect on melittin-induced decrease in mechanical threshold. These experimental findings suggest that verapamil and omega-conotoxin GVIA can inhibit the development and maintenance of melittin-induced nociceptive responses.
