II est bien établi que les hormones sexuelles influencent le développement et la maturation du fœtus. Les travaux classiques de Jost (1947 & 1970), chez le lapin, ont montré que les sécrétions du testicule fœtal contrólent l'organogenèse de l'appareil génital maˇle en stabilisant le développement du canal de Wolff et en induisant la régression du canal de Müller; l'ovaire, par contre, ne jouerait aucun róle dans la différenciation sexuelle du fœtus femelle. On sait, par ailleurs, que la maturation et la sexualisation de certaines parties du système nerveux central sont contrólées, pendant la période périnatale, par des hormones stéroïdes (Gorski, 1971). L'étude de la nature des stéroïdes impliqués dans ces processus a été abordée récemment et la testostérone a pu ětre mesurée dans la gonade fœtale chez le mouton (Attal, 1969), le rat (Warren et al, 1973; Bloch et al, 1974), l'homme (Huhtaniemi et al, 1970; Reyes et al, 1973) et le singe (Resko, 1970). Les travaux relatifs au dosage de la testostérone circulante chez le fœtus, sont également peu nombreux : le singe (Resko et al., 1973), l'homme (Mizuno et al., 1968; Abramovich & Rowe, 1973; Reyes et al., 1974), les bovins (Challis et al., 1974), les ovins (Strott et al, 1974) et les porcins (Meusy-Dessolle, 1974). Chez les espèces dans lesquelles le róle du testicule embryonnaire dans la différenciation sexuelle a été le mieux étudie : lapin (Jost, 1947), souris (Raynaud & Frilley, 1947), rat (Wells & Fralick, 1951), la mesure des androgènes circulants n'a pu ětre réalisée, probablement en raison de la taille des embryons. Chez le lapin, par exemple, si l'aptitude du testicule fœtal à synthétiser des androgenès, et notamment de la testostérone a été bien établie par Lipsett & Tullner (1965), Goldman et al (1972) et Wilson & Siiteri (1973), il n'existe pas de données concernant leur dosage dans les gonades ou le plasma.
Experiments were designed to examine the influence of either one or both parents on the sexual maturation of male mice. A pregnant female and an adult vasecto-mized male were housed together and, at delivery, the litter was reduced to 6 pups, 3 of each sex. After weaning, mother, foster-father or both, stayed in cohabitation with their pups until sacrifice. The results showed that : (1) the permanent presence of one or both parents did not affect either testicular growth or the age at first fertile matings. (2) in maturing males (30–40 days), seminal vesicle growth was accelerated by the presence of the mother, inhibited by the presence of the foster-father. (3) in maturing males, the presence of one or both parents lowered plasma testosterone levels. On the opposite, in 90-day-old males, the same conditions increased testosterone levels.
This paper is concerned with hormonal regulation of the developmental pattern of major proteins of the mouse vas deferens (mouse vas deferens protein: MVDP, 34.5 kD) and seminal vesicle (15.5, 120 and 140 kD) whose expression is regulated by testosterone at adulthood. The ontogeny of these proteins, studied by SDS-polyacrylamide gel electrophoresis, appeared to be uncoordinated. MVDP was not accumulated until animals were 20 days old and its concentration increased sharply from 20 to 30 days of age. In seminal vesicle, the 15.5 kD protein did not accumulate before day 30 whereas 120 and 140 kD proteins appeared and accumulated between 30 and 40 days. In 30-day-old mice castrated at birth or treated with cyproterone acetate over 29 days, MVDP levels were not abolished and were similar to those measured in 20-day-old males. Testosterone administration, from 1 to 10 days of age, did not induce precocious expression of MVDP. These results suggest that the neonatal expression of MVDP is independent of androgens. In seminal vesicle, the first expression of the 3 proteins studied was dependent upon testicular androgens as shown by neonatal castration and injection experiments. The marked increase in the levels of the 4 proteins studied, during sexual maturation, was not associated with quantitative or qualitative changes in tissular androgen concentrations, suggesting that other factors may be necessary for protein expression. Whereas thyroxine may induce a precocious accumulation of MVDP, prolactin had no stimulatory effect on the accumulation of proteins from vas deferens and seminal vesicle. The results suggest that during sexual maturation gene activation by androgens was progressive.
Plasma testosterone, LH and FSH levels were determined and correlated with reproductive organs growth, testicular differentiation, fighting and mounting behaviour in maturing rabbit. An infantile phase of development extends from birth to 40 days, characterized by low testosterone and FSH levels, decreasing LH levels (until 20 days) and by a slow growth of testis and seminal vesicle. The peripubertal phase starts abruptly around day 40. It is marked by simultaneous events: the appearance of mature Leydig cells in the testis, a striking increase in testosterone and FSH levels, a small rise in LH levels and an acceleration of testicular growth. The phase of rapid growth of seminal vesicle and the first meiotic divisions start around day 70, in presence of high circulating levels of FSH and testosterone. Fighting (3 months) and mounting behaviour (146 +/- 13 days) occur lately after a long period of high circulating testosterone levels.
Young sexually naive (3-4 months) and sexually experienced (2-3 years) male rabbits were subjected to various sexual stimulation procedures. Blood samples were taken just before and 30 min after mounting (unreceptive females) or coitus (receptive females). Testosterone and luteinizing hormone were assayed using specific radioimmunoassays. Sexual stimulation did not affect postcoital testosterone and LH levels in naive and experienced males while in females LH levels were significantly increased. We may conclude that the postcoital neuroendocrine reflex which causes a massive release of pituitary LH in female rabbit does not exist in males.
To determine whether neonatal endogenous androgens influence adult renal androgen binding, newborn male mice were injected from 1 to 10 days of age with cyproterone acetate and newborn females with testosterone from 1 to 10 days and from 20 to 40 days of age. In controls, at adulthood, the total cellular androgen receptor content was significantly higher in males (1700 +/- 200 receptors per cell) than in females (1060 +/- 50) and, as expected, the nuclear receptor content was 12-fold higher in males. While the total number of receptors (1650 +/- 200 per cell) was unchanged in adult males neonatally treated with cyproterone acetate, their distribution between cytosol and nucleus was similar to that in control females despite normal circulating and renal testosterone levels. The nuclear receptors represented 50, 7 and 11% of the total receptors in control males, control females and cyproterone acetate-treated males, respectively. The very low levels of nuclear receptors present in the kidney of cyproterone acetate-treated males probably explain the decreased sensitivity of this organ to testosterone. The nuclear receptor accumulation measured in adult animals after a single injection of testosterone did not seem to be affected by neonatal hormonal manipulations.
Kidneys of adult male mice are larger than those of females because of both cellular hyperplasia and hypertrophy. Administration of testosterone to adult female mice induced cellular hypertrophy but not hyperplasia, so that the weight of the kidney remained smaller than in male mice. The sexual dimorphism in kidney size is not congenital but programmed by neonatal endogenous androgens and expressed between 30 and 40 days of age. Treatment of newborn males with cyproterone acetate and of newborn females with testosterone induced female and male patterns of renal growth respectively. It appears that neonatal endogenous androgens are required to induce the characteristic cellular hyperplasia of the kidneys of male mice. Manipulation of androgen levels during neonatal and prepubertal life was found to affect the growth response of the kidney to androgens in adult male and female mice.
