Effects of Heatshock and Reperfusion on the CA1 and Subiculum of the Hippocampus in the Postischemic Gerbil : Electron Microscopy, Immunocytochemistry and Western Blotting Analysis / 沙鼠經熱休克和腦缺血再灌流後海馬體CA1及海馬下托的超微結構、免疫細胞化學與西方墨漬法研究

碩士 / 國立陽明大學 / 解剖暨細胞生物學研究所 / 93 / Preconditiong of sublethal heatshock may be helpful for cellular protection or tolerance against the following insults. Ischemia causes two effects: hypoxia and hypoglycemia. Ischemia results in lowering the blood flow of the brain and causing the pathological damages. The hippocampus is more vulnerable to ischemic injury of the brain. Ischemia can cause the delayed neuronal death in the sector CA1 of the hippocampus .However, the sector of the CA3 is tolerant for against the ischemic damages. The mechanism is still not elucidated at the present time. The aim of this thesis is to investigate that prior to ischemia (30 min) the effect of the sublethal heatshock treatment (45°C,30min) on the cellular injury and recovery of the subiculum and CA1 region of the hippocampus by GFAP-like and S-100-like immunoreactivity and electron microscopy.
Under the light microscopic study,reperfusion causes a severe injury in the neural cells. The cell can be returned to a normal looking after reperfusion following ischemia. Under the electron microscopic level,the astrocyte show perikaryonic dilation and numerous vacuoles in the cytoplasm. In addition, there are hypertrophied cisternae of the rough endoplasmic reticulum, megamitochondria and well-developed golgi apparatus in the astrocyte. Another striking characteristic are that clumped chromatins and the disruption of the nuclear envelop. At 4 h reperfusion after 30 min ischemia with heatshock pretreatment,majority of the cells appear normal looking, especially in the astrocyte and the oligodendrite. In the severe injured areas of the CA1 region of the hippocampus, S-100 immunolabeled cytoplasmic processes increase in length. The other striking morphological changes are that the collapse of the lumen of the blood vessels and the S-100-like immunoreactive product surrounding the periphery of the blood vessel. GFAP-like IR is peaked at 1 h reperfusion after 30 min ischemia. Based on our present data, GFAP and S-100 may be involved in the regulating the cell death and survival in response to the ischemic insults and heatshock tolerance.

Identiferoai:union.ndltd.org:TW/093YM005391002
Date January 2005
CreatorsShu-Chi Chang, 張舒琪
ContributorsShang-Ming Yu, 游祥明
Source SetsNational Digital Library of Theses and Dissertations in Taiwan
Languagezh-TW
Detected LanguageEnglish
Type學位論文 ; thesis
Format86

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