2001 Fiscal Year Final Research Report Summary
Mechanisms of microglial stress response in injured central nervous tissue
| Project/Area Number |
12671341
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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 |
Cerebral neurosurgery
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| Research Institution | Chiba University |
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Principal Investigator |
YAMAURA Akira Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (40009717)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAKAMI Iwao Chiba University, University Hospital, Lecturer, 医学部・附属病院, 講師 (90241968)
SAEKI Naokatu Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 助教授 (30143275)
MURAI Hisayuki Chiba University, University Hospital, Assistant, 医学部・附属病院, 助手 (80241967)
IWADATE Yasuo Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (70272309)
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| Project Period (FY) |
2000 – 2001
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| Keywords | traumatic brain injury / microglia / astroglia / immunotoxin / neuron |
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| Research Abstract |
As a whole, whether activated microglia are acting as protectors or attackers to the neurons in response to the certain pathological condition such as trauma? In this study we used microglia-specific immunotoxin, Mac-1-SAPORIN, at the time of injury to temporally eliminate microglia to see the effects following penetrating traumatic brain injury in mice.
At 24 hours after injury, very few arborized microglia were observed around the injury site in microglia ablation group, while arborized microglia were widely distributed around the injury site or throughout the ipsilateral hippocampus and round-shaped microglia/macrophage were sparsely distributed along the needle track in microglia non-ablation group. At 7 days after injury, many arborized microglia were observed around the injury site or throughout the ipsilateral hippocampus even in immunotoxin treated (microglia ablation) group. Gliosis around the injury site was more evident in microglia non-ablation group at 72 hours and 7 days following injury. At 72 hours after injury, the neuronal cell loss became evident in the non-ablation group compared to that in ablation group. However, at 7 days after injury, no statistically significant difference was observed.
The microglia ablation with immunotoxin ameliorated the neuronal cell loss in the dentate gyrus following penetrating traumatic brain injury in the mouse hippocampus. The microglia ablation also inhibited the hypertrophic change and proliferation of astrocytes following traumatic brain injury. We concluded that activated microglia in the acute stage of penetrating brain injury are considered to mainly act on the neurons suffering from injury as attackers through their phagocytic function and/or modification of astrocyte-neuron interaction.
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Research Products
(2 results)
