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To test the interaction of androgen and inhibin feedback on the pituitary gland, inhibin-type feedback from the testes was reduced when they were made aspermatogenetic by bilateral ligation of the efferent ducts or local heating (43 °C for 30 min). There were only minor effects on the subsequent response of the pituitary gland to the removal of androgen feedback by the administration of antiserum against testosterone or by castration. However, in the antiserum-injected animals the steroidogenic response of the testis to the increased serum concentrations of LH was less in aspermatogenic than in control rats. Furthermore, unilateral aspermatogenesis was associated with reduced testosterone output by the treated testis and with compensatory increased output by the contralateral control testis, despite the absence of significant changes in serum LH and normal peripheral levels of testosterone. This suggests that the tubules can regulate the responsiveness of the Leydig cells to LH.
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The acute effects of a specific reduction in androgen feedback to the hypothalamus and pituitary gland have been investigated in male rats by passive immunization against testosterone. An ovine antiserum raised against testosterone which had been conjugated through position 3 to bovine serum albumin was employed.
Negative feedback control by androgens was effectively reduced by administration of the antiserum, as shown by an increase in levels of LH in the circulation. Immunized animals had a high concentration of testosterone in the circulation of which virtually all was tightly bound to antibody.
In normal animals specific increases of serum LH concentration were obtained at all ages using a low dose of antiserum. At higher doses, serum FSH concentration was also increased. The LH response was reduced by anaesthesia and sham-operation. In shamoperated rats given a high dose of antiserum for 3 days the serum concentrations of LH and FSH could not be distinguished from those which followed castration while differences were found in the pituitary contents. It was concluded that testicular androgen provides an important inhibitory feedback control of secretion of FSH as well as that of LH in the adult male rat. Some of the data can best be explained by the action of inhibin as a minor or alternative inhibitor of FSH secretion.
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Spermatogenesis in rats was interrupted by local X-irradiation, heat or ligation of the testicular efferent ducts. A significant and specific rise in the serum level of FSH occurred 5–8 days after ligation of the efferent ducts, reaching twice the value observed in shamoperated controls by 21 days after the operation. After the testes were heated to 43 °C for 30 min, the serum levels of both LH and FSH were raised within 3 days and remained so up to 50 days after treatment. After X-irradiation, no changes in the concentration of FSH were observed in the first 21 days after treatment, but the serum levels of both gonadotrophins were increased at 49 days. By comparing the relative increases in the concentrations of FSH and LH after germ cell damage with those occurring after castration, it was evident that testicular androgens could account for only part of the normal feedback control of FSH secretion; at least one third of the inhibition of FSH secretion appeared to be due to non-androgenic sources, presumably 'inhibin'.
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ABSTRACT
The physiological roles of chicken LHRH-I and -II (cLHRH-I and -II) in the regulation of gonadotrophin release were investigated in the domestic chicken. Measurements of the neuropeptides, using specific radioimmunoassays, in brain sections cut in three planes or in grossly dissected brain areas, showed that cLHRH-II occurs in low amounts throughout the brain whereas cLHRH-I is most abundant in the diencephalon. Within the diencephalon, the largest amount of cLHRH-I occurred in the median eminence of the hypothalamus. The amount of cLHRH-I in the median eminence was higher (P<0·05) in laying than in out-of-lay hens. No cLHRH-II was detected in the median eminence in either reproductive state. The amount of cLHRH-I in the hypothalamus was increased (P<0·05) in cockerels at the onset of puberty and in somatically immature birds after castration. There were no correlated changes in the amounts of hypothalamic cLHRH-II measured in the same experimental samples.
Active immunization of laying hens against cLHRH-I but not against cLHRH-II resulted in the complete regression of the reproductive system and a depression in the concentration of plasma LH.
These observations, taken together, suggest that gonadotrophin secretion in the hen is more likely to be directly regulated by cLHRH-I than by cLHRH-II.
Journal of Endocrinology (1990) 124, 291–299
