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COMPARISON OF NICOTINIC ANTAGONISTS IN BLOCKING THE EFFECT OF ANATOXIN-A AND NICOTINE ON THE MOTOR ACTIVITY OF RATS.
Citation:
MACPHAIL, R. C., J. D. FARMER, AND K. JAREMA. COMPARISON OF NICOTINIC ANTAGONISTS IN BLOCKING THE EFFECT OF ANATOXIN-A AND NICOTINE ON THE MOTOR ACTIVITY OF RATS. Presented at Society of Toxicology, San Diego, CA, March 05 - 09, 2006.
Description:
Anatoxin-a is a potent nicotinic agonist produced by many species and genera of cyanobacteria. Previous research showed that both anatoxin-a and nicotine produce dose-related decreases in the motor activity of rats. The two toxins differed, however, in their effects with weekly administration; tolerance and sensitization developed with nicotine whereas no change in effectiveness occurred with anatoxin-a. These results suggest differences in the site(s) of action of anatoxin-a and nicotine. We therefore determined the effectiveness of nicotinic antagonists in blocking the decreases in motor activity produced by anatoxin-a and nicotine. Motor activity was measured in commercial photocell devices during 20-min sessions with adult male Long Evans rats. In each experiment groups of 9 rats received subcutaneous injections of either (1) saline vehicle, (2) the centrally acting antagonist mecamylamine (1 mg/kg) or the peripherally acting antagonist hexamethonium (10 mg/kg), (3) the agonist anatoxin-a (0.6 mg/kg) or nicotine (2.5 mg/kg), or (4) a combination of antagonist followed by agonist. Antagonists were given 20-min and agonists were given 5-min prior to testing. Doses were based on prior dose-response determinations. Both anatoxin-a and nicotine decreased motor activity. Mecamylamine pretreatment blocked the decrease produced by nicotine but not anatoxin-a. Hexamethonium did not block the effect of either anatoxin-a or nicotine. Collectively, these results affirm that nicotine?s effect on motor activity is centrally mediated whereas the effect of anatoxin-a appears to involve a novel site(s) of action.
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