| Project/Area Number |
17390062
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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 |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Waseda University |
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Principal Investigator |
NAGASHIMA Kei Waseda University, Faculty of Humansciences, Professor (40275194)
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| Co-Investigator(Kenkyū-buntansha) |
KABE Akiyoshi Waseda University, Faculty of Humansciences, Associate Professor (80367086)
TOKIZAWA Ken Waseda University, Faculty of Humansciences, Lecturar (00454083)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥15,230,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥630,000)
Fiscal Year 2007: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2006: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2005: ¥9,500,000 (Direct Cost: ¥9,500,000)
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| Keywords | thermoregulation / the suprachismatic nucle / brown adipose tissue / UCP1 / Clock mutation / hypothalamus / cFos / daily torpor / 時計遺伝子 / 体温 / 温度感受性ニューロン |
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| Research Abstract |
The goal of present study was to clarify the mechanism involved in generation of circadian body temperature rhythm. In the research, we hypothesized that 1) the suprachiasmatic nucleus (SCN), i. e. the central for circadian rhythms modulates thermosensitiveity at the levels of the central and periphery, and 2) the body temperature rhythm is important in synchronizing the rhythms of the central and periphery. In experiments, mice were exposed to the cold at 20℃ after ad-lib feeding or 48-h fasting, then we estimated metabolic heat production and UCP1 mRNA in the brown adipose tissue. In addition, cFos expression reflected by neural activity in the hypothalamus was also estimated. The same experimental protocol was repeated on Clock mutant mice, which lacks normal circadian rhythmicity. During ad-lib feeding, there were no differences in thermoregulatory responses and cFos expression in the cold. However, during fasting, heat production response was apparent only in the dark phase, and cFos expression in the SCN was augmented in the light phase. There were no phase-differences in the responses in Clock mutant mice. We also found an inhibitory network from the SCN and paraventricular nucleus associated with the sympathetic nerve activity. The SCN was influenced by environmental temperature and feeding condition, which is involved in time-dependency of body temperature regulation.
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