Linked Life Data

7753400

Source:http://linkedlifedata.com/resource/pubmed/id/7753400

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pubmed-article:7753400pubmed:dateCreated1995-6-21lld:pubmed
pubmed-article:7753400pubmed:abstractTextInduction of heat shock/stress proteins is a key feature of a universal mechanism of cellular defence to injury known as the "stress response". The present study investigated whether heat shock protein expression correlates with the extent of neuronal injury inflicted by increasingly intense seizure activity. Limbic epilepsy was elicited by injecting intraperitoneally 8, 10 or 12 mg/kg kainic acid in adult Sprague-Dawley rats, resulting in graded degrees of seizure intensity and duration that closely correlated with the respective dose. Stress protein expression was investigated by immunocytochemistry and western blot analysis of microdissected brain areas with specific antibodies directed against representative members of three major classes of stress proteins, i.e. heat shock protein 72, heat shock protein 90 and heat shock protein 27, respectively. Heat shock protein 72 was absent in the brains of control animals, but markedly induced after limbic seizures in neurons of the limbic system, cortex, striatum and thalamus, with peak levels at 24 h. An increasing degree of seizure intensity caused a graded increase of heat shock protein 72 levels with a sequence reflecting the rank order of kainic acid susceptible hippocampal subpopulations. In contrast to heat shock protein 72, heat shock protein 90 was markedly expressed and equally abundant in all brain areas of untreated control animals and at any time point investigated following limbic seizures. Heat shock protein 27 was not detected in the brain of untreated animals nor following epilepsy. The present investigations demonstrate that the induction threshold of heat shock protein 72 in specific neuronal subpopulations clearly correlates with seizure intensity and duration. In addition, our experiments also define a narrow range of heat shock protein 72 expression with an upper limit beyond which heat shock protein 72 synthesis sharply declines. These findings reflect the risk of hippocampal neurons to undergo limbic seizure induced neuronal degeneration. It remains to be determined whether heat shock protein 72 expression is only a valuable marker for reversible neuronal injury or actually confers a neuroprotective effect.lld:pubmed
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pubmed-article:7753400pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:7753400pubmed:year1995lld:pubmed
pubmed-article:7753400pubmed:articleTitleCorrelation between seizure intensity and stress protein expression after limbic epilepsy in the rat brain.lld:pubmed
pubmed-article:7753400pubmed:affiliationInstitute of Neuropathology, University of Heidelberg, Germany.lld:pubmed
pubmed-article:7753400pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7753400pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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