1990 Fiscal Year Final Research Report Summary
Ischemic Neuronal Damage and Excitatory Amino Acid Neurotransmitter
| Project/Area Number |
63570687
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Teikyo University School of Medicine |
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Principal Investigator |
KIRINO Takaki Teikyo Univ. School of Med., Associate Prof., 医学部, 助教授 (10161605)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAGI Kiyoshi Teikyo Univ. School of Med., Assistant Prof., 医学部, 講師 (40197059)
GOTOH Osamu Teikyo Univ. School of Med., Assistant Prof., 医学部, 講師 (40134598)
TAMURA Akira Teikyo Univ. School of Med., Professor, 医学部, 教授 (80111532)
TAKUSAGAWA Yutaka Teikyo univ. School of Med., Assistant Pro (10179591)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Cerebellum / Purkinje's cell / Granule cell / Ischemia / Cell death / Neurotransmitter / Glutamate |
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| Research Abstract |
Transient global ischemia was induced for 10 min in the rat by raising the intracranial pressure higher than the systemic arterial blood pressure. The animals were perfusion-fixed at 3h, 6h, 12h, 1d, 2d, or 4d following the ischemic insult. Ischemic neuronal alteration was always found in the cerebellum throughout the observation period. The change in the hippocampus was only seen in the specimen obtained 4d after ischemia. Three hours following ischmia, Purkinje's cells looked darkly stained to basic dyes such as toluidine blue and hematoxylin. Six hours after ischemia, darkly Stained Purkinje's cells were more than half of the whole Purkinje's cell population. Dark staining was observed throughout the Purkinje's cell including cell body, nucleus, and dendrite. The inside structure of the dark Purkinje's cell was well maintained and there was no empty swelling or condensation of the cell organelles. Twelve hours after ischemia and later, darkly stained cell disappeared and whole Purkinje's cell number remained unchanged. Two days following ischemia, 25% decrease of Purkinje's cell number was seen. In hematoxylin-eosin stained specimen at this stage, acidophilic neurons were scattered in the Purkinje's cell layer. In the granule cell layer, swollen Purkinje's cell axon was seen from 3h through 4d specimens. The results indicate that dark cell change is, at least partially, a reversible type of ischemic alteration. Following ischemia, unlike hippocampus, Purkinje's axon is involved in the development of ischemic neuronal damage. There seem to be difference in the distribution of excitatory neurotransmitter receptors between the hippocampus and cerebellum. The morphological difference found here may be a reflection of the diversity in receptor subtype distribution.
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