Linked Life Data

1833527

Source:http://linkedlifedata.com/resource/pubmed/id/1833527

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-11-21
pubmed:abstractText
Glutamate-induced delayed neurotoxicity has been proposed to account for the selective loss of hippocampal pyramidal neurons after an ischemic period. We have studied the effects of exogenous glutamate and combined oxygen-glucose deprivation on the survival of hippocampal pyramidal neurons cultured from rat fetuses. Acute glutamate neurotoxicity (20 min, 23-25 degrees C) occurred in a concentration-dependent manner (LD50: 50 microM), destroying virtually all neurons 24 hr later. Such injury was prevented by N-methyl-D-aspartate (NMDA), but not non-NMDA, antagonists. Hippocampal cell death induced by removal of oxygen and glucose showed a similar pharmacological profile, indicating a role for NMDA receptor activation in neuronal loss associated with this energy crisis situation. Monosialogangliosides such as GM1 were effective in protecting against neurodegeneration induced by either direct glutamate exposure or oxygen and glucose deprivation. The selective action of gangliosides in disrupting the pathological consequences of glutamate receptor activation may provide a new therapeutic tool for excitatory amino acid-related brain injury processes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
259
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
452-7
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Death of cultured hippocampal pyramidal neurons induced by pathological activation of N-methyl-D-aspartate receptors is reduced by monosialogangliosides.
pubmed:affiliation
Fidia Research Laboratories, Abano Terme, Italy.
pubmed:publicationType
Journal Article