Abstract
Studies have suggested that the neuroprotective actions of alpha7 nicotinic agonists arise from activation of receptors and not from the extensive desensitization which rapidly follows activation. Here, we report that the alpha7-selective nicotinic antagonist, methyllycaconitine (MLA), protects against beta-amyloid-induced neurotoxicity; whereas the alpha4beta2-selective antagonist, dihydro-beta-erythroidine, does not. These findings suggest that neuroprotective actions of alpha7-acting agents arise from receptor inhibition/desensitization and that alpha7 antagonists may be useful neuroprotective agents.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Aconitine / analogs & derivatives*
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Aconitine / antagonists & inhibitors
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Aconitine / pharmacology
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Amyloid beta-Peptides / toxicity*
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Animals
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Animals, Newborn
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Brain / cytology
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Cell Death / drug effects
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Cells, Cultured
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Dose-Response Relationship, Drug
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Drug Interactions
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Mice
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Neurons / drug effects*
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Nicotinic Antagonists / pharmacology*
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Peptide Fragments / toxicity*
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Receptors, Nicotinic / metabolism*
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Tetrazolium Salts
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Thiazoles
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alpha7 Nicotinic Acetylcholine Receptor
Substances
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Amyloid beta-Peptides
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Chrna7 protein, mouse
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Nicotinic Antagonists
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Peptide Fragments
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Receptors, Nicotinic
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Tetrazolium Salts
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Thiazoles
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alpha7 Nicotinic Acetylcholine Receptor
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amyloid beta-protein (1-42)
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methyllycaconitine
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thiazolyl blue
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Aconitine