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NICOTINE-RECEPTOR BLOCKADE AND THE EFFECTS OF ANATOXIN-A ON THE MOTOR ACTIVITY OF RATS: COMPARISON WITH NICOTINE.
Citation:
JAREMA, K., J. D. FARMER, AND R. C. MACPHAIL. NICOTINE-RECEPTOR BLOCKADE AND THE EFFECTS OF ANATOXIN-A ON THE MOTOR ACTIVITY OF RATS: COMPARISON WITH NICOTINE. Presented at Society of Toxicology, Charlotte, NC, March 26 - 29, 2007.
Description:
Anatoxin-a is produced by several species of freshwater cyanobacteria and has caused several poisoning episodes in terrestrial and aquatic wildlife, livestock and domestic animals. Anatoxin-a is also a potent nicotinic agonist in the nervous system and at the neuromuscular junction. There has been little research on the behavioral effects of anatoxin-a, and virtually no characterization of the role of nicotinic receptors. These experiments determined the effects and interactions of anatoxin-a and selective nicotinic-receptor antagonists on the motor activity of adult male Long Evans rats. Parallel studies included nicotine. Motor activity was evaluated in a commercial photocell chamber during 20-min sessions. Each experiment included groups of 9 rats that received a dose of anatoxin-a or nicotine, a dose of a nicotinic antagonist, and their combination. Each experiment also included a vehicle-control group. Doses of anatoxin-a and nicotine were 0.6 mg/kg and 2.5 mg/kg, respectively, and were administered s.c. 5-min prior to a test session. Nicotinic antagonists included dihydro-beta-ethroidine (DHBE, 10 mg/kg) and methyllycaconitine (MLA, 10 mg/kg). MLA was given s.c 15-min prior to testing and DHBE was given immediately before anatoxin-a or nicotine. Pretreatment with DHBE produced a transient blockade of the effect of nicotine, but did not block the effect of anatoxin-a. Pretreatment with MLA blocked the effect of anatoxin-a, but not that of nicotine. These results indicate anatoxin-a differs from nicotine in its site of action, most likely involving stimulation of alpha-7 nicotinic receptors in the nervous system.