Abstract
Nicotinic acetylcholine (nAChR) and N-methyl-D-aspartate receptors (NMDARs) play critical roles in memory function. This study administered chronic nicotine to determine the alterations of N-methyl-D-aspartate receptor subunit 2A and 2B (NR2A, NR2B) and the alterations of alpha7nAChR receptor. It was determined that the effectivity of nicotine and the data support that nicotine increases hippocampal NR2A and B expression. Additionally, the role of nicotine in the cognitive improvement was not supported by the antioxidative mechanisms or the authors observed no effect of nicotine on lipid peroxidation at the hippocampus.
MeSH terms
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Age Factors
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Aging
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Animals
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Blotting, Western
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Cognition / drug effects
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Ganglionic Stimulants / administration & dosage
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Ganglionic Stimulants / pharmacology*
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Hippocampus / drug effects*
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Hippocampus / metabolism*
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Lipid Peroxidation / drug effects
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Nicotine / administration & dosage
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Nicotine / pharmacology*
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / drug effects*
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Receptors, Nicotinic / drug effects*
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Receptors, Nicotinic / metabolism*
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alpha7 Nicotinic Acetylcholine Receptor
Substances
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Chrna7 protein, rat
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Ganglionic Stimulants
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NR2B NMDA receptor
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Receptors, N-Methyl-D-Aspartate
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Receptors, Nicotinic
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alpha7 Nicotinic Acetylcholine Receptor
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Nicotine
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N-methyl D-aspartate receptor subtype 2A