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 in | Neurotoxicology and teratology Vol. 27; no. 4; pp. 593 - 598 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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New York, NY
Elsevier Inc
01.07.2005
Elsevier Science |
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Abstract | 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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AbstractList | 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. 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. 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 microg/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. |
Author | Chernoff, N. MacPhail, R.C. Farmer, J.D. Jarema, K.A. |
Author_xml | – sequence: 1 givenname: R.C. surname: MacPhail fullname: MacPhail, R.C. email: macphail.robert@epa.gov organization: Neurotoxicology Division, U.S. Environmental Protection Agency, 109 TW Alexander Drive, MD B105-03, Research Triangle Park, NC 27711, United States – sequence: 2 givenname: J.D. surname: Farmer fullname: Farmer, J.D. organization: Neurotoxicology Division, U.S. Environmental Protection Agency, 109 TW Alexander Drive, MD B105-03, Research Triangle Park, NC 27711, United States – sequence: 3 givenname: K.A. surname: Jarema fullname: Jarema, K.A. organization: Neurotoxicology Division, U.S. Environmental Protection Agency, 109 TW Alexander Drive, MD B105-03, Research Triangle Park, NC 27711, United States – sequence: 4 givenname: N. surname: Chernoff fullname: Chernoff, N. organization: Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, 2525 Chapel Hill-Nelson Highway 54, MD 67, Research Triangle Park, NC 27711, United States |
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Keywords | Activity Anatoxin-a Mice Cyanobacteria Nicotine Agonist Rodentia Biological activity Alkaloid Vertebrata Mammalia Mouse Animal Bacteria |
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SubjectTerms | Activity Analysis of Variance Anatoxin-a Animals Animals, Newborn Bacterial Toxins - toxicity Bacteriology Behavior, Animal - drug effects Biological and medical sciences Cyanobacteria Dose-Response Relationship, Drug Drug Interactions Female Fundamental and applied biological sciences. Psychology Male Marine Toxins - toxicity Medical sciences Mice Microbiology Microcystins Motor Activity - drug effects Neurotoxins - toxicity Nicotine Nicotine - pharmacology Nicotinic Agonists - pharmacology Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pregnancy Prenatal Exposure Delayed Effects Tobacco, tobacco smoking Toxicology Tropanes |
Title | Nicotine effects on the activity of mice exposed prenatally to the nicotinic agonist anatoxin-a |
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