Antagonists of NMDA Receptor, Calcium Channel and Protein Kinase C Potentiate Inhibitory Action of Morphine on Responses of Rat Dorsal Horn Neuron.
- Author:
Hong Kee SHIN
1
;
Yeon Suk KIM
;
Jong Hun JUN
;
Seo Eun LEE
;
Jae Hwa KIM
Author Information
1. Department of Physiology, College of Medicine, Hanyang University, Seoul 133-791, Korea. shinhg@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Dorsal horn neuron responses;
Morphine-induced inhibition;
Calcium channel antagonist;
NMDA receptor antagonist;
Protein kinase C inhibitor
- MeSH:
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine;
Animals;
Calcium Channels*;
Calcium*;
Horns;
Morphine*;
N-Methylaspartate*;
Posterior Horn Cells*;
Protein Kinase C*;
Protein Kinases*;
Rats*;
Verapamil
- From:The Korean Journal of Physiology and Pharmacology
2003;7(5):251-254
- CountryRepublic of Korea
- Language:English
-
Abstract:
he present study was designed to examine whether the co-application of morphine with Ca2+ channel antagonist (Mn2+, verapamil), N-methyl-D-aspartate (NMDA) receptor antagonist (2-amino-5-phosphonopentanoic acid[AP5], Mg2+) or protein kinase C inhibitor (H-7) causes the potentiation of morphine- induced antinociceptive action by using an in vivo electrophysiological technique. A single iontophoretic application of morphine or an antagonist alone induced weak inhibition of wide dynamic range (WDR) cell responses to iontophoretically applied NMDA and C-fiber stimulation. Although there was a little difference in the potentiating effects, the antinociceptive action of morphine was potentiated when morphine was iontophoretically applied together with Mn2+, verapamil, AP5, Mg2+ or H-7. However, the potentiating action between morphine and each antagonist was not apparent, when the antinociceptive action evoked by morphine or the antagonist alone was too strong. These results suggest that the potentiating effect can be caused by the interaction between morphine and each antagonist in the spinal dorsal horn.
