| Project/Area Number |
60440046
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Niigata University |
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Principal Investigator |
IKUTA Fusahiro Niigata Univ., Brain Research Inst., Professor,, 脳研究所, 教授 (20018592)
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| Co-Investigator(Kenkyū-buntansha) |
OYANAGI Kiyomitsu Niigata Univ., Brain Research Inst., Assist.,, 脳研究所, 助手 (00134958)
TAKEDA Shigeki Niigata Univ., Brain Research Inst., Assist.,, 脳研究所, 助手 (90134957)
YOSHIDA Yasuji Niigata Univ., Brain Research Inst., Assist.,, 脳研究所, 助手 (70126465)
OHAMA Eisaku Niigata Univ., Brain Research Inst., Ass. Prof.,, 脳研究所, 助教授 (50018892)
山崎 一徳 新潟大学, 脳研究所, 助手 (60115087)
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥19,200,000 (Direct Cost: ¥19,200,000)
Fiscal Year 1987: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1986: ¥4,800,000 (Direct Cost: ¥4,800,000)
Fiscal Year 1985: ¥12,000,000 (Direct Cost: ¥12,000,000)
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| Keywords | Brain edema / Lesion repair / Edema fluid / Viral Cell / Mitosis of astrocyte / Embryonal brain development / Development of blood vessels / 反応性血管 / アストロサイト / 細胞外間隙 / 細胞 / 移動運動 / 胎児脳 / 細胞分裂 |
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| Research Abstract |
Based on a chronological examination of cold lesions, we suggested that the condition, "edema", could be considered to be essential for lesion repair and that it is actually compatible to the physiolgical environment seen in the fetal developing brain (Acta Neuropathol. Suppl. VIII, 103, 1983).
We further studied the experimentally induced edema by various pathological factors including ischemia, trauma, intoxication (organic mercury) and viral infection (SSPE). On the edema and astrocyte activitites in the repair process, all of these lesions showed fundamentally same morphological alterations as those in the cold lesions.
In the first stage, neuronal degeneration and severe swelling of the astrocytes were noticed. In the second stage, when tissue damage was severe enough, hematogenous edema fluid permeated the extracellular space. Thus, all neurons and astrocytes were freely floating in the edema fluid, which provides a significant space for cell motility. In the third stage, macrophages appeared in the fluid and phagocytized necrotized cell debris. Simultaneously, the astrocytes showed mitosis and acquired the ability of motility. After all cell debris was removed, the lesions proceeded to the fourth and final stage of lesion repair. Surviving neurons, synapses and blood vessels were again covered by the processes of postmitotic "reactive" astrocytes.
In mild lesions, however, the first stage of swelling of the astrocytes continued and permeation of edema fluid was either not evident. The necrotized neurons appeared to be removed or digested mostly by the astrocytes.
Interestingly mitosis of the astrocytes was found in the lesions from the third to fourth day exclusively, regardless of the severity of the lesion.
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