Selective Damage of Hippocampal CA1 Neurons Following Transient Forebrain Ischemia in Rats: Protection by Postischemic Application of NMDA Receptor Antagonist
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概要
- 論文の詳細を見る
Transient forebrain ischemia in rats produces a characteristic pattern of selective damage in the brain, leading pyramidal neurons in the CA1 region of the hippocampus to delayed cell death 3-4 days after reperfusion. Recent reports suggest that glutamate release of two distinct phases (during ischemia and after ischemia) produces the delayed cell loss of CA1 neurons, raising a question whether glutamate released during ischemia serves only to cause a susceptibility to glutamate released after ischemia. To examine whether glutamate receptor antagonist when given after ischemia exhibits a perfect protection against the delayed damage of hippocampal CA1 neurons, N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801) was administered recurrently in rats over 4 days after transient ischemia by 4-vessel occlusion method. Fifteen minutes of forebrain ischemia produced a wide spectrum of neuronal cell loss selectively in the hippocampal CA1 area. Postischemic application of MK-801 reduced significantly the delayed damage of hippocampal CA1 neurons following the 15 min of transient forebrain ischemia, but the protective effect was not perfect, still remaining the small population (18%) of cell loss of CA1 neurons.
- 鳥取大学の論文
著者
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Saji Makoto
Department Of Physiology School Of Allied Health Sciences Kitasato University
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Saji Makoto
Department Of Neurobiology Faculty Of Medicine Tottori University
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Saji Makoto
Department Of Neurobiology Faculty Of Medicine And Gene Research Center Tottori University
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