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ABSTRACT
The temporal release of testosterone by Leydig cells from 18-day-old mouse fetuses in response to human chorionic gonadotrophin (hCG) and to 8-bromo-cyclic AMP (8-bromo-cAMP) was investigated under short-term incubation (180 min) conditions. A rapid and large increase in testosterone release was induced by a 5-min exposure to hCG (20 i.u./l) or 8-bromo-cAMP (10 mmol/l). The testosterone response of fetal Leydig cells to the two gonadotrophic stimuli was Gaussian in distribution with a peak value of testosterone by 15–20 min. Repeated exposure to hCG resulted in a reduced testosterone response but an increased accumulation of cAMP. The apparent resistance of fetal Leydig cells to hCG could not be overcome either by increasing the hCG concentration (to 2000 i.u./l) or by exposing the cells to 8-bromo-cAMP (10 mmol/l). Continuous exposure to hCG (200 i.u./l) divided into multiple small doses (each 8 i.u./l) induced testosterone secretion with different kinetic characteristics: a three-fold longer time-lag between hormone exposure and the peak value; a twofold greater testosterone response (P<0·001) and a gradual decrease of testosterone secretion. Oestradiol significantly reduced basal and hCG-stimulated testosterone production only at a high concentration (10 μmol/l). These results indicate that continuous or pulsatile exposure to hCG can induce refractoriness of fetal Leydig cells. The similarity between the actions of hCG and 8-bromo-cAMP on fetal steroidogenesis suggests that this rapid defect is not primarily due to a depletion of gonadotrophin receptors but results from disruption of regulatory mechanisms at the post-receptor level.
J. Endocr. (1985) 107, 409–414
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Laboratoire de Chimie Hormonale Maternité de Port-Royal, 75014 Paris, France and †Centre de Recherches Endocrinologiques, Hôpital Cochin, 27 rue du Faubourg St-Jacques, 75014 Paris, France
(Received 31 January 1977)
It has been suggested that testosterone production by the foetal testis is under gonadotrophin control (Catt, Dufau, Neaves, Walsh & Wilson, 1975; Warren, Haltmeyer & Eik-Nes, 1975), but the particular roles of foetal pituitary and/or chorionic gonadotrophin are not clearly understood. We have previously demonstrated that a substance with both the biological and radioimmunological properties of luteinizing hormone (LH) is present in the pituitary gland of the male mouse foetus at 18 days of gestation (Pointis & Mahoudeau, 1976a, b). In the present work, we attempted to determine whether the pituitary gland of the male mouse foetus exhibits gonadotrophic activity during earlier stages of genital tract differentiation.
On days 14-18 of gestation, the gonads and pituitary glands of male foetuses (Albino
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Levels of testosterone in plasma and concentrations of LH in both plasma and pituitary glands of fetal mice aged 14, 16 and 18 days were measured by radioimmunoassays in a representative number of fetuses. During this period levels of testosterone in the plasma of male mice were significantly higher than those in the females. Levels of testosterone in plasma of male mice increased from day 14 to day 16 of gestation and decreased on day 1 before parturition. Plasma concentrations of LH remained undetectable in male and female fetuses until day 16 of gestation. Levels of LH rose slightly in both sexes in later gestation, but still remained significantly lower in the plasma of male fetuses on days 17–18. In contrast, higher but not significantly different concentrations of LH were observed in pituitary glands from days 14 to 18 in male compared with female mice. These observations suggest that the high levels of testosterone in the plasma of male fetal mice might be responsible for feedback inhibition of LH secretion during the last days of gestation.
