碩士 / 國立陽明大學 / 解剖暨細胞生物學研究所 / 91 / Ischemia may result from impair of cerebral blood flow and lead to hypoxia and hypoglycemia, which cause pathological damage of brain. The hippocampus is the most vulnerable area to ischemia injury, and often used as an experimental model. In spite of the hippocampal CA1 presenting the delayed neuronal death after ischemia, the CA3 is more resistant. But the mechanisms are not fully understood, especially the morphological changes. Initial report suggested that the ratio between Bcl-2 and Bax may determinate the cell would be survival or death following apoptosis, and the nitric oxide synthase (NOS) activities may influence the cell function under ischemic condition. The mongolian gerbils were used for this study and followed 90 minutes unilateral or bilateral common carotid arteries occlusion. Transmission electron microscopy and immunocytochemistry of Bcl-2, Bax, nNOS, iNOS and eNOS are used to examine the ultrastructural and morphological change.
Under the light microscope observation, effect of the reperfusion causes more damage in the hippocampal CA3 than in the permanent occlusion, and the morphological changes are progressed following the change of different time course. Under the electron microscope observation, the neurons with high electron densities, which have both apoptotic and necrotic features, including clumped chromatins in nucleus, large vacuoles, dilatation of the mitochondria and rough endoplasmic reticulum in cytoplasm, appears in the hippocampal CA3. Astrocytes and oligodendrocytes also display the chromatin condensation and cytoplsmic lucidification. nNOS- like- IR is similar to that of eNOS, and they are found predominantly in the cytoplasm of pyramidal neurons, whereas iNOS- like- IR in the nucleus. Because of these three isoforms of NOS all found in basophilically, shrunk, darkened neurons, this indicates that they may all participate in the regulation of the neuronal death. On the other hand, Bcl-2 and Bax disappear mostly from these neurons, this implies that there may not directly be related to the mechanism regulating the hippocampal CA3 neuronal death.
| Identifer | oai:union.ndltd.org:TW/091YM000391005 |
| Date | January 2003 |
| Creators | Shih-Wei Wu, 吳詩薇 |
| Contributors | Shing-Ming Yu, 游祥明 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 81 |
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