MECHANISNS OF NEURONAL DEQTH IN THE RAT (SHRSP) CEREBRAL CORTEX FOLLOEING FOCAL PERMANENT ISCHEMIA BY MIDDLE CEREBRAL ARTERY OCCLUSION
MECHANISNS OF NEURONAL DEQTH IN THE RAT (SHRSP) CEREBRAL CORTEX FOLLOEING FOCAL PERMANENT ISCHEMIA BY MIDDLE CEREBRAL ARTERY OCCLUSION
批准号:
07680828
负责人:
NITATORI Tohru
金额:
$1.41万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1995
资助国家:
日本
项目状态:
已结题
起止时间:
1995 至 1997
中文摘要
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英文摘要
The cortical neurons are known to be vulnerable to anoxic, which in neuropathological changes of the neurons within the infarcted area. In the present study, we examined early histo-pathological changes in the cortical neurons after focal cerebrai, ischemia, induced by permanent unilateral occlusion of the middle cerebral artery (MCA). In the experimental animals infarcted cortical neurons within the focal wrea at the territory of MCA rapidly underwent cell death, while the neurins within ischemic penumbra exhibited relatively delayd neuronal death after ischemic insult. It remain, however, undefined whether death of these neurons are necrosis or apoptosis. We examined the degenerating process of the cortical neurons within the focal area and ischemic penumbra of cerebral cortex after focal ischemia. At 2 hrs after ischemic insults neurons within the focal area already changed their feature into relatively expanded shapes. Plasma membrane of these neurons was broken into pieces and fragments of disintegrated organelles scattered whithin cytoplasm. Expanded Nuclei of these broken into pieces and fragments of disintegrated oranelles scattered within cytoplasm. Expanded Nuclei of these neurons expressed TUNEL positive reaction. On the other hand, typical necrotic swelling neurons and highiy electron dense small ones were detected within the ischemic penumbra at 6 frs after ischemia. The latter neurons exhibited cell shrinkage accompanied with an increase in immunoreactivity for iysosmal cystein proteinases. Nuclei of these neurons showed TUNEL positive reacition from 1 to 3 days after insults. Degenerated neurons were heterophagocytosed by phagocytes invaded into the area. These results suggest that aduth death of the cortical neurons within the focal area after focal ischemia by MCA occlusion is necrotic, whereas neuronal death the ischemic penumbra consisted of necrotis and apoptoti.
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Nitatori T. and Y.Uchiyama: "Apoptosis of the CA1 pyramidal neurons after transient ischemia." Recent Advances in Microscopy of Cells, Tissues and Organs. (Motta PM ed.), Malpighi Volumes on Functional Microanatomy, Boston, Kluwer. 177-181 (1997)
Nitatori T. 和 Y.Uchiyama:“短暂性缺血后 CA1 锥体神经元的凋亡。”
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通讯作者:
Nitatori T.and Y.Uchiyama: "Apoptosis of the CA1 pyramidal neurons after transient ischemia." Recent Advances in Microscopy of Cells,Tissues and Organs.(Motta PM ed.),Malpighi Volumes on Functional Microanatomy,Boston,Kluwer.(in press).
Nitatori T. 和 Y.Uchiyama:“短暂性缺血后 CA1 锥体神经元的凋亡。”
DOI:
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发表时间:
期刊:
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作者:
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通讯作者:
Yasuo Uchiyama et al: Ischemic neuronal death, I : The Living and Death of Neuron (H.Hatanaka ed). Toko Kagaku Dojin, 175-180 (1997)
Yasuo Uchiyama 等人:缺血性神经元死亡,I:神经元的生与死(H.Hatanaka 编)。
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通讯作者:
Tohru Nitatori et al: Participation of cathepsins B,H and Lin perikaryal condensation of CAI pyramidal neurons undergoing apoptosis after brief ischemia, In : Intracellular Catabolism (K.Suzuki and J.Bond eds). Prenum Press, 177-185 (1996)
Tohru Nitatori 等人:组织蛋白酶 B、H 和 Lin 参与短暂缺血后经历细胞凋亡的 CAI 锥体神经元的核周凝结,In:细胞内分解代谢(K.Suzuki 和 J.Bond 编辑)。
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通讯作者:
似鳥 徹: "脳虚血とアポトーシス" 総合リハビリテーション. 25巻・10号. 1143-1149 (1997)
Toru Nitori:“脑缺血和细胞凋亡”综合康复,第 25 卷,第 10 期。1143-1149 (1997)
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