Intracisternal Administration of Voltage Dependent Calcium Channel Blockers Attenuates Orofacial Inflammatory Nociceptive Behavior in Rats.
- Author:
Kyoung A WON
1
;
Sang H PARK
;
Bo K KIM
;
Kyoung S BAEK
;
Dong H YOON
;
Dong K AHN
Author Information
1. Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Korea. dkahn@knu.ac.kr
- Publication Type:Original Article
- Keywords:
VDCCs;
orofacial pain;
antinociception;
formalin test
- MeSH:
Adult;
Animals;
Calcium;
Calcium Channel Blockers;
Calcium Channels;
Calcium Channels, L-Type;
Calcium Channels, N-Type;
Calcium Channels, T-Type;
Dihydropyridines;
Facial Pain;
Formaldehyde;
Humans;
Injections, Subcutaneous;
Male;
Mibefradil;
Neurons;
Pain Measurement;
Polyethylene;
Rats;
Rats, Sprague-Dawley;
Verapamil
- From:International Journal of Oral Biology
2011;36(2):43-50
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Voltage dependent calcium channel (VDCC), one of the most important regulator of Ca2+ concentration in neuron, play an essential role in the central processing of nociceptive information. The present study investigated the antinociceptive effects of L, T or N type VDCC blockers on the formalin-induced orofacial inflammatory pain. Experiments were carried out on adult male Sprague-Dawley rats weighing 220-280 g. Anesthetized rats were individually fixed on a stereotaxic frame and a polyethylene (PE) tube was implanted for intracisternal injection. After 72 hours, 5% formalin (50 microL) was applied subcutaneously to the vibrissa pad and nociceptive scratching behavior was recorded for nine successive 5 min intervals. VDCC blockers were administered intracisternally 20 minutes prior to subcutaneous injection of formalin into the orofacial area. The intracisternal administration of 350 or 700 microg of verapamil, a blocker of L type VDCC, significantly decreased the number of scratches and duration in the behavioral responses produced by formalin injection. Intracisternal administration of 75 or 150 microg of mibefradil, a T type VDCC blocker, or 11 or 22 microg of cilnidipine, a N type VDCC blocker, also produced significant suppression of the number of scratches and duration of scratching in the first and second phase. Neither intracisternal administration of all VDCC blockers nor vehicle did not affect in motor dysfunction. The present results suggest that central VDCCs play an important role in orofacial nociceptive transmission and a targeted inhibition of the VDCCs is a potentially important treatment approach for inflammatory pain originating in the orofacial area.
