J Korean Soc Emerg Med.  2004 Dec;15(6):475-486.

Expressions of the pERK1/2 and the cFos Proteins at an Early Stage of Transient Global Ischemia-reperfusion Injury in the Hippocampus of Rats

Affiliations
  • 1Department of Emergency Medicine, Wonkwang University School of Medicine, Iksan, Korea. ysoojin@wmc.wonkwang.ac.kr

Abstract

PURPOSE
This study was to evaluate temporal changes in the expressions of the phosphorylated extracellular-regulated kinase1/2 (pERK1/2), the phosphorylated MAPK/ERK kinase1/2 (pMEK1/2) and the cFos proteins in the hippocampus of rats following transient global ischemia.
METHODS
Transient global ischemia was induced in the forebrains of Sprague-Dawley rats by using a 4-vessel occlusion for 20 min under anesthetic condition. Hematoxyline-eosin staining showed typical microscopic findings that represented neuronal cell death in hippocampal CA1 regions 5 days after transient global ischemia. Four-vessel occlusion-reperfusion produced ischemic injury in major forebrain structures, such as the striatum, the cortex and the hippocampus, in the finding of triphenyltetrazolium chloride (TTC) staining.
RESULTS
A high density of pERK1/2 immunoreactivity existed in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 5 min after ischemia. Following ischemia, expression of the pMEK1/2 protein showed temporal changes similar to that of the pERK1/2 protein. A significant expression of the cFos protein was noted in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 2 hours after global ischemia.
CONCLUSION
Intracellular signaling cascades of the ERK or the cFos protein take part in early cellular events in the hippocampus of rats in response to ischemic insult.

Keyword

Hippocampus; pERK1/2; pMEK1/2; cFos; Transient global ischemia

MeSH Terms

Animals
CA1 Region, Hippocampal
Cell Death
Dentate Gyrus
Hippocampus*
Ischemia
Neurons
Prosencephalon
Rats*
Rats, Sprague-Dawley
Reperfusion Injury*
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