2001 Fiscal Year Final Research Report Summary
Development and evaluation of new kinds of fatigue animal models, and researches on their neural mechanisms and related molecular factors in central nervous system.
| Project/Area Number |
12670145
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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 |
Pathological medical chemistry
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| Research Institution | Osaka City University Graduate School of Medicine |
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Principal Investigator |
NAKAMURA Fusao Osaka City University Graduate School of Medicine, Department of Physiology, Research assistant, 大学院・医学研究科, 助手 (80271196)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Yasuyoshi Osaka City University Graduate School of Medicine, Department of Physiology, Chief Professor, 大学院・医学研究科, 教授 (40144399)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Fatigue / Brain / Forced swim / Behavior / Glucose / Acidosis / compensation |
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| Research Abstract |
This study was aimed to develop new models for fatigue researches and find the regions responsible for the fatigue in the central nervous system. To make adult male SD rats exhaustive, they were set in pipette washers in which water (15℃) went up and down for 30 minutes for modified forced swim (FS). After the FS, it took about 54 minutes for first step and about 84 minutes for glooming and shuddering. Decrease in locomotive distance and velocity, for 30 minutes after the FS also indicated the rats were exhaustive. In this new fatigue model, base excess and pH decreased (metabolic acidosis) for 30 minutes after the FS, with increase in such metabolites as lactate and pyruvate in their blood, followed by respiratory acidosis for about 3 hours with increase in arterial CO_2 pressure (PaCO_2). The mechanism for the fatigue may include the insufficiency of respiratory compensation for the metabolic acidosis due to decrease in glucose uptake into diaphragm. In central nervous system, after the FS, [^<18>F] FDG uptake in the whole brain also decreased. Changes in glucose uptake also differed among the brain region. In pons, medulla oblongata and cerebellum, Fos immunoreactivity increased but relative glucose uptake did not change. In cerebral cortex, cingulate, hippocampus, amygdala and septal region, relative glucose uptake decreased severely in spite of the increase in Fos immunoreactivity. This was also the case in another model of fatigue due to sleep deprivation. Greater decreases in glucose supply in the cerebral cortex and the limbic system may be related to the mechanism of fatigue.
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