2006 Fiscal Year Final Research Report Summary
Does stress promotes neurodegenerative changes?
| Project/Area Number |
17500216
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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 |
Neuroscience in general
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| Research Institution | Nippon Medical School |
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Principal Investigator |
SUGAMA Shuei Nippon Medical School, Faculty of Medicine, Assistant Professor, 医学部, 講師 (70302461)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Makoto Tokyo Metropolitan Institute for Neuroscience, laboratory for Chemistry and Metabolism, Professor, 病態脳, 副参事研究員 (50189502)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Stress / Microglia / Interleukin-18 / Central Nervous System / Neurodegenerative disease / Inflammation |
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| Research Abstract |
The goal of the present study was to investigate the influence of psychological/physical stress on microglial activation. The effect of stress on microglial activation was evaluated in unstressed or after 1 h and 2 h of restraint combined with water immersion stress as well as 6 h after release from the 2 h of stress. Under control conditions, resting microglia characterized by their small somas and long and fine processes were distributed throughout the brain. Following the stress, morphological activation of microglia was observed throughout the brain including the thalamus, hypothalamus, and hippocampus, substantia nigra and central grey surround the 3rd ventricle. Six hours after the stress, morphological activation was still present although diminished. Intriguingly, significant microglial activation was more pronounced in the vicinity of the third ventricle. Stress-activated microglia was not immunoreactive to ED1 or OX-6, suggesting that stress-activated microglia are not involv
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ed in the phagocytic activity. In addition, we measured the levels of IL-lb, IL-6 and iNOS, as functional inflammatory markers of microglia. The result demonstrated that the levels of these ninflammatory markers did not alter during and after the stress, suggesting that inflammation may not be accompanied with the stress-induced microglial activation. Next, to investigate the effect of interleukin-18, we injected recombinant IL-18 in the intraperitoneal space. The result clearly demonstrated that morphological microglial activation occurred following IL-18 inejction. Furthermore, we compared stress-induced microglial activation between wild type and IL-18 knock out mice. The result demonstrated that stress-induced microglial activation was significantly reduced as compared to that of wild type mice. However, stress-induced microglial activation was not completely abolished in IL-18 knock out mice, suggesting that any other factors may trigger stress-induced microglial activation. As a summary, acute stress did not induce inflammatory reactions in the brain. Thus, it is less likely that acute stress, itself, may cause the neuronal damages that are caused by microglial inflammation. Less
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Research Products
(10 results)
