Linked Life Data

10915565

Source:http://linkedlifedata.com/resource/pubmed/id/10915565

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-8-31
pubmed:abstractText
Systemic administration of kainic acid (KA) to rodents results in limbic seizures and subsequent neurodegeneration similar to that observed in certain types of human epilepsy, and it is a commonly used animal model for this disease. Oxidative stress has been suggested to play a role in the neuronal injury associated with KA administration. Based on this observation, chronic treatment with antioxidants has been proposed as a possible protective therapy against neuronal damage associated with epileptic seizures. Here we demonstrate by histochemical, electrophysiological, and biochemical means that knockout mice with decreased activity of the protective antioxidant enzyme glutathione peroxidase, which display elevated basal brain oxidative stress levels, are resistant to KA-induced seizure activity and neurodegeneration. This appears to be a result of decreased NMDA receptor function due to oxidation of its NR1 subunit. This suggests that the chronic use of antioxidants as antiepileptic agents to modulate NMDA-dependent seizure-induced neurodegeneration may be detrimental rather than protective and calls into question their use as a therapeutic agent in the treatment of epilepsy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
257-68
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Chronic brain oxidation in a glutathione peroxidase knockout mouse model results in increased resistance to induced epileptic seizures.
pubmed:affiliation
Division of Neurogerontology, University of Southern California, Los Angeles, California 90089, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.