| Project/Area Number |
18591297
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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 |
Psychiatric science
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| Research Institution | University of Miyazaki |
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Principal Investigator |
UEDA Yuto University of Miyazaki, Faculty of Medicine, Associate Professor (70244192)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Akira University of Miyazaki, Faculty of Medicine, Associate Professor (10041857)
DOI Taku University of Miyazaki, Faculty of Medicine, Research Associate (70274793)
ISHIDA Yasushi University of Miyazaki, Faculty of Medicine, Professor (20212897)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,780,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Glutamate / Redox / GABA / Neonatal isolation / kindling |
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| Research Abstract |
Nitroxide radical has been reported to react with hydroxyl radical and superoxide anion radical in the presence of cysteine or NADH. In this report the EPR SI of nitroxide radicals did not decay exponentially in the reaction with other radicals. The signal decay in this reaction is in accord with a linear function. On the other hand, its EPR SI decayed exponentially in the reaction with the reductants. Therefore, the reaction dynamics of nitroxide radicals with the reductants differed from that with other radicals. In the present study, the EPR SI of hydroxymethyl-PROXYL decayed exponentially. Therefore, the shortening of the halflife in the NI group without acute stress does not arise due to the reaction of nitroxide radical to other radicals (such as superoxide radical and hydroxyl radical). This indicates the enhancement of reducing ability. Therefore, the results obtained in this study indicate that while the intracerebral reducing ability was significantly depleted by acute stress in the NI group, this depletion did not occur in the control rats. It was also found that the intracerebral reducing ability significantly increased in the rats that had been subjected to NI when the acute stress was not applied. It is thought that the in vivo reducing ability is decreased due to mitochondrial damage, and a previous study reported that immobilization stress induced mitochondrial dysfunction. Therefore, the depletion of the intracerebral reducing ability after immobilization in the NI group may be related to mitochondrial damage in the brain. However, interpretation of the mechanisms behind the enhancement of intracerebral reducing ability in the NI group without the acute stress is now under way. We believe that impairment of the intracerebral reducing ability caused by acute stress in the NI rats is important biological evidence of cerebral vulnerability to acute stress in this model.
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