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Vol. 284, Issue 3, 1058-1065, March 1998
Department of Pharmacology and Toxicology Medical College of
Virginia, The objective of this study was to determine which nicotinic receptor
subtypes are involved in antinociception and their site of action. For
that, the antinociceptive effects of several nicotinic receptor ligands
were evaluated in the tail-flick test both after s.c. and intrathecal
(i.t.) administration. Nicotine and other nicotine agonists increased
tail-flick latencies in a dose-dependent manner after both routes of
administration. Epibatidine enantiomers were the most potent agonists
examined. Cytisine, a potent nicotinic ligand, failed to elicit
antinociception when injected either i.t. or s.c. Despite some
similarities in the effects of nicotinic agonists after i.t. and s.c.
injections, their rank-order potency was different. In contrast to the
s.c. results, the stereoselectivity of nicotine's effect after i.t.
administration was minimal. When various nicotinic antagonists were
compared after i.t. and s.c. administration, the results showed that
mecamylamine and dihydro-
-erythroidine differ in potency and their
degree of antagonism of some of the nicotinic agonists given i.t. These
data suggest that different subtypes of nicotinic receptors may exist
in the spinal cord. A good correlation was found between binding
affinity to [3H]-nicotine binding sites and analgesic
potency after i.t. (r = 0.82), suggesting the involvement of
42 receptor subunits. In contrast,
studies with MLA and -BGTX suggested a minimal role for
-BGTXsensitive receptors in the antinociceptive effect of nicotinic
agonists.
0022-3565/98/2843-1058$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics
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