J Korean Neurol Assoc.
1996 Jun;14(2):319-330.
The protective effect of Cortical Infarction to the Neuronal damage following subsequent global ischemic insult in gebril
- Affiliations
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- 1Department of Neurology, College of Medicine, Hallym University, Yonsei University.
- 2Department of Pathology, College of Medicine, Ewha Woman's University.
Abstract
- Prior brief ischemic insult was reported to protect the hippocampal CA1 neurons from delayed neuronal death following global ischemia. Mechanisms of such protective effects have, however, remained unclear. The study was conducted to confirm whether the preceding cortical infarction exerts protective effects on the adjacent hippocampal CA1 neurons against the subsequent global ischemia and to reactive astrocytosis to the mechanisms of protective effects. Male, mongolian gerbils, aged 12-15 weeks and weighing 70-90g, were anethetized with ketamine by intraperitoneal injections, and a small cortical infarction in the unilateral parietal cortex was made by infusing of magnetic ferrite particles which were followed by subsequent global ischemia for 5 minutes on 1, 3 and 7 days later. One week following the subsequent global ischemia, the neuronal degeneration in the hippocampal CA1 regions was examined by Hematoxylin-eosin stain. Immunohistochemistry using GFAP antibody was carried out for evaluating the time course of astrocytic reactivity after 1, 3, and 7 days of cortical infarction. The neuronal degeneration of CA1 regions in the ipsilateral hippocampus preceded by the cortical infarction was less severe than those in the contralateral ones. The differences of neuronal degeneration between both of hemispheres was clearly more prominent in animals whose global ischemia was induced at 1 and 3 days cortical infarctions than 7 days. However, the reactivity of GFAP astrocyte was minimal at 1 day but markedly increased at 3 and 7 days after cortical infarction. This present study confirmed that the preceding cortical infarction may protect the adjacent ipsilateral CA1 neurons from the subsequent global ischemic insult with its protective effect being most remarkable at 1 and 3 days but less at 7 days after cortical infarction. However, the degree of reactive astrocytosis measured by GFAP immunohistochemistry did not correlate well with the degree of neuroprotection, thus it did not fully account for the mechanisms of such protective effect.
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