[Demonstration of the gonadotropic cells of the pituitary gland in the rat by the immunofluorescence method].
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Biomedical subjects
Publications and source records attributed to C Robyn.
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The effects of sudden modifications of extracellular calcium ion concentration on human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) release were investigated using term placental explants incubated in Krebs Ringer solution. The hCG and hPL releases were both stimulated when the extracellular Ca2+ concentration was increased. The hCG and hPL secretions elicited by the addition of extracellular Ca2+ were larger when placental explants were preincubated in alpha-calcium (no added calcium + EGTA) than in normo-calcium (1.5 mM). Removal of extracellular Ca2+ from the medium also elicited an increase in hCG and hPL release. However, this stimulatory effect of Ca2+ omission was partly suppressed by washing the explants prior to incubation in the alpha-calcium medium, and was completely abolished when alpha-calcium medium was supplemented with 1 mM cobalt. Our results indicate that changes in Ca2+ modify hCG and hPL release from term placental explants in a manner concordant with the 'stimulus-secretion coupling' concept.
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Thirty seven mature Mangabeys (Cercocebus atys lunulatus), 33 females (5-6 kg) and 4 males (6-7 kg) received large doses of 17-beta-oestradiol by intravenous tracts (continued perfusion and single dose injection) and by subcutaneous implantation in a silastic tube. The CB 154 and TRH tests under oestrogenic treatment were the object of an integrated study. All these experiments began 5 days after menstruation in the case of the females. The experiments were preceded, for each monkey, by a control period that rarely exceeded 5 days. Prolactin and oestradiol were measured by radioimmunoassay. Single intravenous injection and perfusion of 17-beta-oestradiol were followed by an inconstant effect on the immediate secretion of prolactin (+30 to +60 minutes). However, after 4 to 6 hours, serum prolactin rose by about 50% of the basic ratios. This is followed by a more notable elevation of the blood ratios of PRL during the 24 to 72 hours which succeed the end of the oestradiol treatment. The subcutaneous placing of a silastic tube containing oestradiol is followed by a Systematic fall in the Serum PRL for 9 hours (day 0). During the following 3 weeks, the ratios rise but are situated at a normal level (F = 0.2 p greater than 0.5) in spite of a liberation and maintenance of the serum oestrogen at a very high level. Nevertheless, the peak of PRL following a TRH test under oestrogenic treatment is greater (F = 4.7 p less than 0.05) than the peak obtained during the control period with the same dose of TRH.
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For 21 days, nine male monkeys received daily doses, 8 mg of testosterone propionate dissolved in almond oil. After an initial period of 6 days, a control period was observed during which only the almond oil was administered. Each injection was preceded by the taking of a 10 ml blood sample. The prolactin and steroids (testosterone and oestradiol) were measured by radioimmunoassay. For both groups of animals the prolactin serum count increase significantly after 10 days of treatment. This modest increase (approximately 50% a base count) is more systematic among the immature subject than among the mature ones. The oestradiol serum count increased among the same animals on day + 2 and remained at a noticeably high level from day + 2 to day + 20. These results suggest a stimulatory effect of testosterone on the secretion of prolactin due to the conversion of androgen to oestradiol. However a mild testosterone action directly on lactotropic cells is not to be discounted.
Chronic hyperprolactinaemia was induced in 10 women since the onset of a cycle for 2 or 3 consecutive cycles by administration of sulpiride (3 X 50 mg/day) or tiapride (100-200 mg/day). The resulting perturbations of the menstrual cycle included short luteal phase cycles, anovulatory cycles and amenorrhoea. The analysis of the hormonal profiles under treatment, as compared to the control cycles, indicate an impact of hyperprolactinaemia both preferentially at the hypothalamic (alteration of the secretion or endogenous LRH) and accessorily at the ovarian (lack of progesterone secretion by the near mature follicle) levels.