1985 Fiscal Year Final Research Report Summary
Regulatory Mechanims for Gonadotropin Secretion in Pituitary Cells of Fowl
| Project/Area Number |
59440016
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
畜産学(含草地学)
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| Research Institution | Gifu University |
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Principal Investigator |
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| Project Period (FY) |
1984 – 1985
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| Keywords | Hen pituitary / Gonadotropin / Progesterone-receptor / Estrogen-receptor / Serotonin / <beta> -Endorphin / オピエート・ペプチド |
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| Research Abstract |
Incubations of the hen pituitary cells in vitro with estradiol-17 <beta> caused an increase in progesterone-receptor bindings, and this increase was inhibited by the presence of cycloheximide, actinomycin-D and amanitin. A successive incubation with progesterone casused an increase in the cellular content of LH while the incubation without the preincubation with estradiol-17 <beta> did not cause the increase. It is suggested that the estrogen mayprime the hen pituitary cells for the action of progesterone for the production of LH.
A specific estrogen binding component having the properties of a receptor was found in vitro in both soluble and insoluble fractions of the hen pituitary in a hypotonic buffer solution.
Serotonin and <beta> -endorphin were found to block normal and progesterone-induced ovulation, and to suppress the release of LH from the pituitary in normal and progesteroneinjected hens. An inhibitor of serotonin synthesis caused the release of LH and diminished the effect of <beta> -endorphin. An antagonist of opiate peptides diminished the effect of <beta> -endorphin but not the effect of serotonin. The results suggest that both serotonin and <beta> -endorphin are involved in the control of LH-release in the hen as an inhibitory agent, and serotonin is predominant while <beta> -endorphin is subsidiary to the inhibition of the LH-release in the hen.
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