1999 Fiscal Year Final Research Report Summary
MECHANISM OF NEURONAL DEATH AND REGENERATION
| Project/Area Number |
10470038
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | THE UNIVERSITY OF TOKYO |
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Principal Investigator |
SHIMIZU Takao UNIVERSITY OF TOKYO, GRADUATE SCHOOL OF MEDICINE, PROFESSOR, 大学院・医学系研究科, 教授 (80127092)
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| Co-Investigator(Kenkyū-buntansha) |
TANIGUCHI Masahiko UNIVERSITY OF TOKYO, GRADUATE SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 大学院・医学系研究科, 助手 (70260346)
IZUMI Takashi UNIVERSITY OF TOKYO, GRADUATE MEDICINE, ASSOCIATE PROFESSOR, 大学院・医学系研究科, 助教授 (70232361)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Neuron / Glial cells / Lipid mediators / Platelet-activating factor / Leukotrienes |
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| Research Abstract |
Neuronal survival and death are determined by multiple factors including neuronal activity as well as an influence from surrounding glia. In this project, we focus on various lipid mediators in terms of its ability of interaction between neuron and glia. We found that various lipid mediators are produced by stimuli, and play roles in the network as follows. LPA, produced by various cells, stimulates growth and cell maturation of neuron as well as proliferation of astrocytes. LPA also releases various cytokines and neurotrophis (NGF, BDNF) from astroglia, which activates neuronal cells. PAP is released from neuron by the NMDA stimulation, and acts on microglia. Microglia produces NO, and causes chemotaxis towards neuron, suggesting the role of microglia for repairing neuronal cells. PAF receptor-deficient mice and phospholipase A2 (cPLA2)-deficient mice are established, and their congenic mice are now available by backcrossing. The exact roles of these lipid mediators will be clarified by extensive analyses of their phenotypes.
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