| Project/Area Number |
06670677
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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 |
Neurology
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| Research Institution | Kinki University |
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Principal Investigator |
TAKAHASHI Mitsuo Kinki University School of Medicine, Department of Neurology, Professor, 医学部, 教授 (20028492)
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| Co-Investigator(Kenkyū-buntansha) |
AKANEYA Yukio Osaka University Medical School, Department of Neurophysiology, Staff, 医学部・付属病院, 医員 (40222517)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Parkinsons Disease / MPP neurotoxicity / fatal rat brain / Dopaminergic neuron / NGF / BDNF / Free radical / Interleukin / ドバミナージックニウロン / ドーパミナージックニューロン / パーキンソン病 / coculture / MPP^+ / 酸 / 標的由来神経栄養因子 / 中脳黒質 |
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| Research Abstract |
To study on the mechanism of MPP^+ neurotoxicity against doperminergic neurons (DN), the vulneravility of cultured cells from the ventral mesencephalon of embryonic 17 days rats under MPP^+ was evaluated with free radical, nerve growth factor, or interleukin.
We have shown that DN may be exclusively sensitive to elevated acidity elicited after the addition of glial mitogenic factors such as epidermal growth factor and basic fibroblast growth factor or after the direct treatment with hydrochloric acid.
The acid sensitivity was specific to DN and was inhibited by addition of brain-derived neurotrophic factor (BDNF).
Such antioxidants as VE,VC,CoQ_<10> and catalase, but neither allopurinol nor superoxide dismutase, alleviated the MPP^+ induced death of DN,while glutamate receptor did not alter MPP^+ neurotoxicity.
Concerning interleukin (IL), IL-1beta was showed to act as a neurotrophic factor on DN,and IL-6 was revealed to be able of protecting DN from the neurotoxicity of MPP^+ without glial proliferation.
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