Nicotine effects on the activity of mice exposed prenatally to the nicotinic agonist anatoxin-a

Anatoxin-a is a nicotinic agonist produced by several genera of cyanobacteria, and has caused numerous deaths of wildlife, livestock and domestic animals world-wide. Several studies in the literature have shown that exposure of mice and rats to nicotine early in development alters its effects when t...

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Published inNeurotoxicology and teratology Vol. 27; no. 4; pp. 593 - 598
Main Authors MacPhail, R.C., Farmer, J.D., Jarema, K.A., Chernoff, N.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.07.2005
Elsevier Science
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Summary:Anatoxin-a is a nicotinic agonist produced by several genera of cyanobacteria, and has caused numerous deaths of wildlife, livestock and domestic animals world-wide. Several studies in the literature have shown that exposure of mice and rats to nicotine early in development alters its effects when the rodents are subsequently challenged with nicotine. We therefore determined the effect of nicotine on the motor activity of adult mice that had been exposed prenatally to anatoxin-a. Pregnant CD-1 mice received either saline vehicle or one of two doses of (+/−) anatoxin-a (125, 200 ug/kg), i.p., on GD13–17. As adults (8 months), control mice of both genders were used to determine the effect of nicotine (0, 0.1, 0.3, 1.0 or 3.0 mg/kg, s.c.) on motor activity measured for 30-min in a photocell device. Under these conditions, nicotine produced dose-related decreases in both horizontal and vertical activity, with an ED50 estimated to be 0.65 mg/kg. Next, additional control mice and mice exposed prenatally to anatoxin-a received the nicotine ED50 and saline vehicle, in a counterbalanced fashion, with one week separating treatments. Nicotine decreased both horizontal and vertical activity in all mice, regardless of prenatal anatoxin-a treatment. Thus, no enduring effects of prenatal anatoxin-a were obtained in adult mice following nicotine challenge.
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ISSN:0892-0362
1872-9738
DOI:10.1016/j.ntt.2005.05.004