Abstract
Maternally lead (Pb)-exposed, juvenile rats exhibit significant deficits in spatial reference memory acquisition and working memory performance in the Morris water maze (MWM). Acute systemic application of nicotine reverses these deficits without affecting behavioral performance of the age-matched, lead-unexposed control animals. These results suggest that nicotinic agonist treatments can ameliorate learning and memory impairments, presumably by compensating for deficient nicotinic function in developmentally lead-exposed animals.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Newborn
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Brain / drug effects*
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Brain / pathology
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Brain / physiopathology
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Disease Models, Animal
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Female
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Lead Poisoning, Nervous System, Childhood / drug therapy*
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Lead Poisoning, Nervous System, Childhood / physiopathology
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Maze Learning / drug effects
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Maze Learning / physiology
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Memory Disorders / chemically induced*
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Memory Disorders / drug therapy*
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Memory Disorders / physiopathology
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Memory, Short-Term / drug effects
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Memory, Short-Term / physiology
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Nicotine / pharmacology*
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Nicotine / therapeutic use
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Nicotinic Agonists / pharmacology
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Nicotinic Agonists / therapeutic use
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Pregnancy
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Prenatal Exposure Delayed Effects*
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Rats
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Reaction Time / drug effects
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Reaction Time / physiology
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Receptors, Nicotinic / drug effects
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Receptors, Nicotinic / physiology
Substances
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Nicotinic Agonists
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Receptors, Nicotinic
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Nicotine