Involvement of melatonin in the inhibition of gonadotropin secretion by stress and its mechanism
Project/Area Number |
10670072
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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Research Institution | St. Marianna University |
Principal Investigator |
AKEMA Tatsuo St.Marianna University School of Medicine, Department of Physiology, Professor, 医学部, 教授 (60128585)
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Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Hitoshi St.Marianna University School of Medicine, Department of Physiology, Research Associate, 医学部, 助手 (70301596)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
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Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
Keywords | Stress / Luteinizing hormone / Naloxone / Melatonin / Bacterial endotoxin |
Research Abstract |
(1) The site where melatonin inhibits gonadotropin secretion. Intraventricular injection of melatonin inhibited naloxone-induced, but not NMDA- or LHRH- induced, LH release. The results showed that the site of melatonin action is located downstream to the site of opioid action and upstream to that of exciatory amino acid action in the hypothalamic LHRH neural network. (2) Effects of various kinds of stress on naloxone-induced LH release. Naloxone-induced LH release was significantly inhibited by acute immobilization stress or infectious stress, moderately inhibited by 3-day fasting , and not affected by 24-hour fasting or footshock stress. (3) Correlation between LH suppression and pineal melatonin release after various kinds of stress. No significant correlation was found between the degree of inhibition of nalloxone-induced LH release and plasma melatonin concentration in rats undergoing various kinds of stress described above. (4) Involvement of the pineal in the inhibition of naloxone-in
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duced LH release by various kinds of stress. Pinealectomy partially restored naloxone-induced LH release after acute immobilization stress, indicating a role of the pineal gland. No obvious effect of pinealectomy was found in rats with other kinds of stress. (5) The site where infections stress inhibits gonadotropin secretion. Intravenous injection of LPS inhibited naloxone-induced and NMDA-induced, but not LHRH-induced, LH release. The results showed that the site of LPS action is located downstream to the sites of action of opioid and excitatory amino acid in the hypothalamic LHRH neural network. Intense c-fos expression was found in ependymal cells (tanycytes) of the posteroventral portion of the third ventricle after the LPS injection. (6) Other factors. Intraventricular injection of IL-1β did not inhibit naloxone-, NMDA- or LHRH- induced LH release, suggesting that mechanism(s) not mediated by IL-1β is, at least in part, involved in inhibition of gonadotropin secretion by infectious stress, acute immobilization and melatonin. Less
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Report
(3 results)
Research Products
(15 results)