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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
1998-7-7
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pubmed:abstractText |
Rats were subjected to transient global ischemia (four vessel occlusion) and time-related changes in the selectively vulnerable hippocampal field CA1 were characterized. The assessment included ex vivo field responses to afferent stimulation, silver staining, calpain-induced spectrin breakdown, chromatolysis, and cell death, beginning at 6 h post-ischemia and continuing until total disintegration of the pyramidal cells occurred several days later. The earliest change observed was a modest increase in the slope and amplitude of field CA1 potentials (at 6 h). The hyperresponsiveness was most apparent at higher stimulation currents and persisted unchanged at 16 h post-ischemia. Three effects became detectable within 24 h, post-ischemia: (a) an increase in concentrations of calpain-mediated, spectrin breakdown products; (b) enhanced silver staining in the deep pyramidal neurons of the field CA1 with lesser, though still apparent, staining of stratum radiatum, and (c) a decrease in amplitude and slope of field CA1 responses to afferent stimulation. Both the concentration of spectrin breakdown products and the intensity of silver staining progressively increased to a maximum at four days post ischemia, while the amplitude and slope of the field responses dropped to a very low level between 24 and 48 h. Disturbances of Nissl staining were finally evident at 48 h, with nearly complete disappearance of staining at five days post-ischemia. This study provides the first demonstration of a close and early temporal relationship between calpain proteolysis, subcellular damage to the pyramidal cells and their loss of function following global ischemia, prior to their eventual death.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1998 Elsevier Science B.V.
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
790
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1-13
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:9593800-Animals,
pubmed-meshheading:9593800-Brain Chemistry,
pubmed-meshheading:9593800-Calpain,
pubmed-meshheading:9593800-Cell Death,
pubmed-meshheading:9593800-Cytoskeleton,
pubmed-meshheading:9593800-Excitatory Postsynaptic Potentials,
pubmed-meshheading:9593800-Hippocampus,
pubmed-meshheading:9593800-Ischemic Attack, Transient,
pubmed-meshheading:9593800-Neurons,
pubmed-meshheading:9593800-Rats,
pubmed-meshheading:9593800-Rats, Sprague-Dawley,
pubmed-meshheading:9593800-Silver Staining,
pubmed-meshheading:9593800-Spectrin,
pubmed-meshheading:9593800-Time Factors
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pubmed:year |
1998
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pubmed:articleTitle |
Temporal ordering of pathogenic events following transient global ischemia.
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pubmed:affiliation |
Alkermes, 64 Sidney Street, Cambridge, MA 02139, USA. rtbartus@alkermes.com
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pubmed:publicationType |
Journal Article
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