Ultrastructural and BDNF-, GFAP-like Immunocytochemical Alterations in Postischemic Dendate Gyrus of Gerbils

碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 92 === Ischemia results from the reduction in the cerebral blood flow and decrease in the oxygen and glucose of brain causing pathological damage of brain due to hypoxia and hypoglycemia. Hippocampus and stratum are the most vulnerable area to ischemic injury. The...

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Bibliographic Details
Main Authors: Hui-Ru Hsu, 徐慧如
Other Authors: Shang-Ming Yu
Format: Others
Language:zh-TW
Published: 2004
Online Access:http://ndltd.ncl.edu.tw/handle/42078790772247133636
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Summary:碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 92 === Ischemia results from the reduction in the cerebral blood flow and decrease in the oxygen and glucose of brain causing pathological damage of brain due to hypoxia and hypoglycemia. Hippocampus and stratum are the most vulnerable area to ischemic injury. The Mongolian gerbils were used for this study. The gerbil were followed 90 minutes bilateral common carotid artery occlusion. The morphological changes and quantitative analysis of the dentate gyrus in the hippocampus followed by artery occlusion and reperfusion in the different time courses had been employed by electron microscopy, BDNF- and GFAP-immunocytochemistry and Western blotting. At the light microscope findings, the reperfusion after 90 min ischemia not only caused more damage in granular cells, but also recovered to normal looking appearance. Under the electron microscope observation, the electron-dense granule cells had indented nucleus, clumped chromatins, disintegration of the nuclear membrane, round protrusion of the perinuclear cisternae of the nuclear and enlarged mitochondria in the cytoplasm. After reperfusion, neurons had shown karyopyknosis and karyorrhexis indicative of apoptotic and necrotic features, respectively. In addition, empty spaces were found among the granules and spongy appearances of vacuoles were located in the subgranular zone corresponded to edematous dendrites. At the onset of reperfusion after 90 min ischemia, GFAP-like-IR markedly increased to peaked level, then decreased after reperfusion. GFAP-like-IR increased drastically at 2 h after reperfusion. BDNF-like-IR were mainly localized in the cytoplasm of the large granule cells and not found in the shrunken, more darker granule cells and elongated, slightly stained cells. A striking feature was that BDNF-like-IR were found in the first appearance and more pronounced in the neural processes at 2 h reperfusion after 90 min ischemia. Another striking characteristic was that many small neurons were intensely immunolabeled by BDNF staining in the subgranular zone at the onset after 90 minutes of both left and right common carotid artery occlusion, after 30 minutes and 18 hours reperfusion. The present data suggests that GFAP and BDNF may be involved in regulating the mechanism of the cell death and survival of the granule cells in the dentate gyrus directly or indirectly.