Summary. Male voles reared in a stimulatory (long) photoperiod have significantly greater contents of hypothalamic Gn-RH and pituitary LH and greater testicular and seminal vesicle weights than do voles reared in inhibitory (short) photoperiods. The inhibitory effects of short photoperiod were reversed by pinealectomy.
E. Versi, Sharon A. Chiappa, G. Fink and H. M. Charlton
E. Versi, Sharon A. Chiappa, G. Fink and H. M. Charlton
Summary. There was a drop of 56% in the hypothalamic content of Gn-RH in female voles 5 min after mating compared with that in unmated but receptive animals. This suggests that the surge of LH in vole plasma associated with reflex ovulation is evoked by a massive release of Gn-RH.
G. Fink, W. J. Sheward and T. M. Plant
Summary. Saline extracts of pituitary glands from normal and hpg male mice were assayed for LH by the testosterone production assay. The extract of hpg pituitary tissue stimulated testosterone production by mouse Leydig cells in a dose-dependent manner which paralleled that of normal mouse pituitary. The normal mouse pituitary was about 20 times as potent as hpg pituitary which is similar to the relative potency obtained by radioimmunoassay. These results show that differentiation of the gonadotrophs and the synthesis of some biologically active LH can occur in the absence of LHRH.
D. M. G. Halpin, A. Jones, G. Fink and H. M. Charlton
Summary. Significant uterine growth occurred in normal and hypogonadal (hpg) mice between Days 7 and 21 but thereafter no further growth was observed in hpg mice. The ovaries of hpg mice were significantly smaller than those of normals at all ages, but there was no significant difference between the number of non-growing follicles in the ovaries of mutants and their normal littermates at any age studied, and normal and hpg mice showed a marked reduction in the number of non-growing follicles during the first month of life. The size and composition of the growing follicle population in hpg mice, however, differed markedly from those in normal animals and by 21 days of age the number of growing follicles in mutants was significantly reduced. There was no significant difference in the number of Type 3b follicles before 60 days of age, but the number of all other follicle types was significantly less in hpg mice at all ages studied. Follicles in which the antrum is fully developed (Type 7 and 8) were never seen in the ovaries of mutants and corpora lutea were never observed. Interstitial tissue development was also very poor in hpg ovaries.
The hypothalamic GnRH content in normal mice remained low until Day 20, before rising sharply to adult levels (∼800 pg) between Days 20 and 30. The pituitary FSH content increased over the first 10 days of life to reach a peak of about 5000 ng, before declining to the adult value of about 2000 ng by Day 30, whilst the plasma FSH concentration was high in the first 10 days, but fell to adult levels over the next 20 days. Pituitary LH content increased significantly between Days 5 and 10 to reach the adult level of about 600 ng.
Hypothalamic GnRH was undetectable at all ages in hypogonadal mice, but the pituitary content of FSH and LH had risen to the attenuated mutant adult value by Day 15, and unlike normals, plasma FSH concentrations were not elevated during the neonatal period.
These results suggest that minimal gonadotrophic stimulation of the ovary from birth has no effect on the total number of follicles but reduces the number of growing follicles and prevents follicle growth beyond the early antral stage. Gonadotrophins therefore appear to have a role in the initiation and continuance of follicle growth in the adult mouse.
K. BROWN-GRANT, G. FINK, FENELLA GREIG and M. A. F. MURRAY
Male rats given 250 μg oestradiol benzoate by subcutaneous injection on Day 4 of postnatal life showed a marked delay in the onset of the pubertal increase in the weight of the testes and seminal vesicles and in spermatogenesis but not a complete failure of sexual development. The increase in plasma testosterone concentration at puberty was also delayed in oestrogen-treated males but the eventual increase in seminal vesicle weight was closely related in time to the delayed increase in plasma testosterone concentration. Both plasma LH and FSH concentrations were reduced for about 10 days after oestrogen administration as compared to control values. After 22 days of age, plasma LH concentration did not differ significantly from the control values. The plasma FSH concentration of the oestrogen-treated males showed a delayed rise to values equal to or higher than those of controls of the same age. The delayed rise in plasma FSH concentration in the oestrogen treated males preceded the delayed rise in plasma testosterone in these animals. The decrease in plasma FSH concentration from the high prepubertal values to the lower values in adults occurred at different ages in the control and in oestrogen-treated rats but in both groups the decrease occurred as plasma testosterone levels were increasing and the first wave of spermatogenesis was reaching completion. The increase in plasma FSH concentration after castration was reduced in oestrogen-treated males during the period throughout which FSH levels in the intact animals were subnormal but the levels in oestrogen-treated males castrated after the delayed rise in FSH had occurred did not differ from control values. It is suggested that the delayed sexual maturation of male rats treated with high doses of oestrogen in the neonatal period is related principally to abnormalities in the secretion of FSH.
L. J. D. ZANEVELD, G. F. B. SCHUMACHER, H. FRITZ, E. FINK and E. JAUMANN
Human sperm acrosomal proteinase is immediately inhibited by the Fraction I (mol. wt. 12,700) and Fraction II (mol. wt. 5,400) proteinase inhibitors of human seminal plasma. The Fraction II inhibitor inhibits acrosomal proteinase much more effectively than the Fraction I inhibitor, having an association constant of 5·0 × 108 m −1 and a dissociation constant of 2 ·0 × 10 − 9 m. The results provide further evidence for the possible rôle of the Fraction II inhibitor in the reproductive process.