| Project/Area Number |
05671193
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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 | Kinki University |
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Principal Investigator |
KATAOKA Kazuo Kinki University school of medicine, Associate professor, 医学部, 講師 (10221178)
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| Co-Investigator(Kenkyū-buntansha) |
TANEDA Mamoru Kinki University school of medicine, Professor, 医学部, 教授 (10236713)
KONDOH Sumio Kinki University school of medicine, Assistant professor, 医学部, 助手 (30225619)
井奥 匡彦 近畿大学, 医学部, 教授 (80088541)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Brain damage / Cerebral infarction / Neural function / Neuronal network / Neurotrophic factor / 大脳皮質 / 視床 / 線条体 / 黒質 / マイクログリア |
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| Research Abstract |
Damage of cortex results in progressive degeneration in the ipsilateral thalamus. Ischemic damage to the striatum leads to remote pathological changes in the ipsilateral substantia nigra. It has been expected that these degenerations are improved by neurotrophic factors or neural transplant. We studied the metabolic, functional and morphological changes in the thalamus or the substantia nigra following cortical damage or striatal damage, respectively. We also studied the effects of basic fibroblast growth factor (b-FGF), one of neurotrophic factors, on the thalamic neurons.
Cortical ablation resulted in degeneration of the thalamus in rats. Single unit recording revealed depression of synaptic transmission in the thalamic neurons after cortical ablation. The b-FGF ameliorated the thalamic degeneraiton, however, the synaptic transmission of the thalamic neurons was not improved by the b-FGF.Cortical infarction also caused degeneration of the thalamus in rats. Deoxyglucose autoradiographic study showed abnormal hypermetabolism of the thalamus in the chronic stage (1 month after cortical infarction) following hypometabolism in the acute stage (3,7 days after cortical infarction) in rats. Immunohistochemical study suggested that this hypermetabolism of the thalamus was attributed to the microglial reaction. Striatal infarction resulted in transneuronal degeneration of the substantia nigra in rats. We also observed glucose hypermetabolism in the ipsilateral substantia nigra 7 days after striatal infarction. However, Single unit recording showed no hyper-exciting substantia nigra neurons 7 and 14 days after striatal infarction.
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