Project/Area Number |
07680828
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | IWATE MEDICAL UNIVERSITY |
Principal Investigator |
NITATORI Tohru IWATE MEDICAL UNIVERSITY, SCHOOL OF MEDICINE LECTURER, 医学部, 講師 (90128934)
|
Co-Investigator(Kenkyū-buntansha) |
佐藤 昇 大阪大学, 医学部, 助手 (00254756)
|
Project Period (FY) |
1995 – 1997
|
Project Status |
Completed (Fiscal Year 1997)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | NEURONAL DEATH / APOPTOSIS / NECROSIS / FOCAL CEREBRAL ISCHEMIA / PENUMBRA / CASPASE / CYSTEINE PROTEINASES / CPP32 / 遅延型細胞死 / ICE / TUNEL反応 |
Research Abstract |
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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