Abstract
We studied the mechanism of antagonism of p-chloroamphetamine-induced neurotoxicity by dextromethorphan. The pretreatment with potent and selective sigma receptor ligands, 4-phenyl-4-(1-phenylbutyl)piperidine (4-PPBP) and N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-ethylamine monohydrochloride (NE-100), did not alter the reduction of 5-hydroxytryptamine and 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the cerebral cortex by repeated administration of p-chloroamphetamine. These results suggest that sigma receptors might not play a significant role in the antagonism of p-chloroamphetamine-induced neurotoxicity by dextromethorphan.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anisoles / pharmacology
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Antitussive Agents / pharmacology
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism*
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Dextromethorphan / pharmacology
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Haloperidol / analogs & derivatives
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Haloperidol / pharmacology
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Hydroxyindoleacetic Acid / metabolism
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Ligands
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Male
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Propylamines / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, sigma / physiology*
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Serotonin / metabolism
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Serotonin Agents / toxicity*
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p-Chloroamphetamine / antagonists & inhibitors
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p-Chloroamphetamine / toxicity*
Substances
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Anisoles
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Antitussive Agents
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Ligands
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Propylamines
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Receptors, sigma
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Serotonin Agents
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4-phenyl-1-(4-phenylbutyl)piperidine
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N,N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)ethylamine monohydrochloride
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Serotonin
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Hydroxyindoleacetic Acid
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p-Chloroamphetamine
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Dextromethorphan
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Haloperidol