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pubmed-article:21070252pubmed:abstractTextAlcohol consumption during pregnancy can damage the developing fetus, illustrated by central nervous system dysfunction and deficits in motor and cognitive abilities. Binge drinking has been associated with an increased risk of fetal alcohol spectrum disorders, likely due to increased episodes of ethanol withdrawal. We hypothesized that overactivity of the N-methyl-D-aspartate (NMDA) receptor during ethanol withdrawal leads to excitotoxic cell death in the developing brain. Consistent with this, administration of NMDA receptor antagonists (e.g., MK-801) during withdrawal can attenuate ethanol's teratogenic effects. The aim of this study was to determine whether administration of memantine, an NMDA receptor antagonist, during ethanol withdrawal could effectively attenuate ethanol-related deficits, without the adverse side effects associated with other NMDA receptor antagonists.lld:pubmed
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pubmed-article:21070252pubmed:copyrightInfoCopyright © 2010 by the Research Society on Alcoholism.lld:pubmed
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pubmed-article:21070252pubmed:articleTitleAdministration of memantine during ethanol withdrawal in neonatal rats: effects on long-term ethanol-induced motor incoordination and cerebellar Purkinje cell loss.lld:pubmed
pubmed-article:21070252pubmed:affiliationDepartment of Psychology, Center for Behavioral Teratology, San Diego State University, California 92120, USA.lld:pubmed
pubmed-article:21070252pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21070252pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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