SPINAL CORD CELL DEATH AFTER EXPERIMENTAL COMPRESSION INJURY IN RATS 7.
| Project/Area Number |
07671605
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
YONE Kazunori Kagoshima University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (40182844)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHINO Shinji Kagoshima University, University Hospital, Research Associate, 医学部・附属病院, 助手 (10274820)
SAKOU Takashi Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (10041295)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | spinal cord injury / neuronal cell death / apoptosis / necrosis |
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| Research Abstract |
Following laminectomy, the spinal cord was injured at T9 segment by extradural static weight-compression using a cylindrical compressor in rats, inducing complete and irreversible transverse spinal cord injury with paralysis of the lower extremities. The injured rats were sacrificed at between 30 minutes and 14 days after injury, and the injured cord was removed en bloc. Rats treated with N-methyl-D-aspartate receptor antagonist (MK-801) were sacrificed at the same time-points as non-treated rats. The spacimens were stained with hematoxylineosin and Nissl stained, and subjected to in situ nick-end labeling, a specific in situ method for visualization of apoptosis.
Thirty minutes after injury, a large hematoma was observed at the compressed segment. Six hours after injury, large numbers of dead cells not stained by in situ nick-end labeling were observed. Between 12 hours and 14 days after injury, nuclei stained by in situ nick-end labeling were observed not only at the site of injury but also in adjoining segments that had not been damaged mechanically, suggesting that the delayd cell death was due to apoptosis.
The number of cells stained by in situ nick-end labeling was maximal 3 days after injury.
The results of electron microscopy were also consistent with apoptosis. In the rats treated with MK-801, the number of cells stained by in situ nick-end labeling was smaller than in non-treated rats at both 24 hours and 3 days after injury.
These findings suggest that excitatory amino acids is one of the promoting factors of delayd neuronal and glial cell death due to apoptosis.
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Report
(4 results)
Research Products
(13 results)
