| Project/Area Number |
11671099
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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 |
Endocrinology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
SHIBASAK Tamotsu Nippon Medical School, Faculty of Medicine, Professor, 医学部, 教授 (00147399)
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| Co-Investigator(Kenkyū-buntansha) |
OHATA Hisayuki Nippon Medical School, Faculty of Medicine, Instructor, 医学部, 助手 (80256924)
ARAI Keiko Nippon Medical School, Faculty of Medicine, Assistant Professor, 医学部, 講師 (60277118)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | corticotropin releasing factor / stress / tail pinch / urocortin / food intake / conditioned fear / paraventricular nucleus of the hypothalamus / noradrenaline / corticotropin-releasing factor / CRF受容体 / CRF受容体拮抗薬 / 視床下部 / ストレス反応 / 覚醒 |
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| Research Abstract |
One minute-tail pinch increased food intake in 30 min, and the effect was blocked by corticotropin-releasing factor (CRF) receptor type 1 (CRFR1) selective antagonist. Intracerebroventricular (icv) injection of CRF Increased and decreased food intake at doses of 2 ng and 1 μg, respectively. These results suggest that slight release of CRF is involved in tail pinch-induced food intake. In addition, we found that dopamine and opioid systems also participate in tail pinch-inducedfood intake.
Urocortin inhibited food intake in rats when it was microinjected to the ventromedial nucleus of the hypothalamus (VMH), and the effect was not affected by CRFR1 antagonist. The microinjection of anti-urocortin γ-globulin to the bilateral VMH increased food intake. Therefore, it is suggested that urocortin in the VMH has an inhibitory effect on food intake, and that the effect is not mediated by CRFR1.
Conditioned fear increased noradrenaline release in the paraventricular nucleus (PVN) of hypothalamus, and the change was blocked by CRFR1. It is therefore concluded that CRFR1 participates in conditioned fear-induced noradrenaline release in the PVN.
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