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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
1997-12-16
|
| pubmed:abstractText |
Alcohol exposure during development can produce central nervous system dysfunction, resulting in a wide range of behavioral alterations. The various mechanisms by which alcohol causes these behavioral changes, however, remain unknown. One mechanism that has been suggested is NMDA receptor-mediated excitotoxic cell death produced by ethanol withdrawal. The present study examined whether MK-801, an antagonist of the NMDA receptor that has been shown to protect against NMDA receptor-mediated excitotoxicity, could block alcohol's adverse effects on behavior. Sprague-Dawley rat pups were exposed to alcohol (6.0 g/kg) in a binge-like manner on postnatal day 6 using an artificial rearing procedure. Subjects then received an injection of MK-801 (0.1 mg/kg) or vehicle during withdrawal, 21 hr after ethanol exposure. At postnatal day 40, all subjects were tested on a serial spatial discrimination reversal task. Ethanol-exposed subjects were impaired in both discrimination and reversal learning, and committed a significantly greater number of perseverative-type errors, compared with controls. MK-801 administration during ethanol withdrawal significantly attenuated ethanol-induced deficits in reversal learning and increases in perseverative-type errors, whereas MK-801 exposure by itself had no significant effect on performance. Thus, exposure to MK-801 during ethanol withdrawal partially protected against alcohol-related disruptions in spatial reversal learning. These results support the suggestion that NMDA receptor-mediated excitotoxicity may be one mechanism by which alcohol induces behavioral teratogenicity.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0145-6008
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
21
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1218-25
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9347082-Alcohol Withdrawal Delirium,
pubmed-meshheading:9347082-Animals,
pubmed-meshheading:9347082-Animals, Newborn,
pubmed-meshheading:9347082-Behavior, Animal,
pubmed-meshheading:9347082-Brain,
pubmed-meshheading:9347082-Discrimination Learning,
pubmed-meshheading:9347082-Dizocilpine Maleate,
pubmed-meshheading:9347082-Female,
pubmed-meshheading:9347082-Fetal Alcohol Syndrome,
pubmed-meshheading:9347082-Humans,
pubmed-meshheading:9347082-Infant, Newborn,
pubmed-meshheading:9347082-Male,
pubmed-meshheading:9347082-Maze Learning,
pubmed-meshheading:9347082-Mental Recall,
pubmed-meshheading:9347082-Neonatal Abstinence Syndrome,
pubmed-meshheading:9347082-Orientation,
pubmed-meshheading:9347082-Pregnancy,
pubmed-meshheading:9347082-Rats,
pubmed-meshheading:9347082-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:9347082-Reversal Learning
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
MK-801 administration during ethanol withdrawal in neonatal rat pups attenuates ethanol-induced behavioral deficits.
|
| pubmed:affiliation |
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|