| Project/Area Number |
09660318
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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 |
Basic veterinary science/Basic zootechnical science
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| Research Institution | NAGOYA UNIVERSITY |
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Principal Investigator |
SAITO Noboru Nagoya University, School of Agriculture, Assistant Professor, 農学部, 助手 (40211924)
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| Co-Investigator(Kenkyū-buntansha) |
FURUSE Mitsuhiro Kyushu University, School of Agriculture, Associate Professor, 農学部, 助教授 (30209176)
SHIMADA Kiyoshi Nagoya University, School of Agriculture, Professor, 農学部, 教授 (40065579)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | chicken / RIA / hypothalamus / arginine vasotocin / osmotic stimulation / opioid peptide / antisense / intracerebroventricular injection / クローニング / 子宮 / AVTmRNA / ATVReceptor / chicken / hypothalamus / osmoregulation / neurohypophysis |
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| Research Abstract |
Arginine vasotocin (AVT) is one of neurohypophyseal hormone in the birds. It is well known that AVT has an antidiuretic action and is released by hypertonic stimulation, but it is little information about the release mechanism of AVT.The aim of this study investigates the release mechanisms of AVT and compares the mechanism between birds and mammals.
When the chickens were received hypertonic saline, the plasma levels of AVT significantly increased. When chickens were received simultaneously with hypertonic saline and opioid peptide, morphine, the increase of plasma levels of AVT was inhibited. On the other hands, when the chickens were received simultaneously with hypertonic saline and opioid peptide antagonist, naloxone, the increase of plasma levels of AVT was further enhanced. From these results, we can suggest that opioid peptide may regulate AVT release by hypertonic stimulation. However, AVT release at oviposiiton were not effected by opioid antagonist or agonist.
The intracerebroventricular injection of AVT antisense oligonucleotide inhibited the increase of plasma levels of AVT by hypertonic stimulation. The intracerevelo injection of AVT sense or random oligonucleotide did not inhibit the increase of plasma levels of AVT by hypertonic stimulation. Antisense oligonucleotide may inhibit translation to amino acid from AVT mRNA within the AVT synthesis mechanism. Therefore, these data may support that AVT biosynthesis mechanism involves the mechanism of AVT release from the neurohypophysis. Also, these data suggest that antisense oligonucleotide is useful tool for the study of neuroendocrinology in birds.
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