Roles of FSH and testosterone in the initiation of spermatogenesis in prepubertal rats medically hypophysectomized by a GnRH antagonist.

Abstract

Experimentally induced medical hypophysectomy in prepubertal rats through treatment of GnRH antagonist for 3 weeks, initiated on the 20th day of age, markedly decreased testicular weight by 85% of that of the controls. Quantitative assessment of spermatogenesis in testicular semithin preparations revealed a significant reduction in the numbers of preleptotene (27.2 +/- 1.6 to 15.6 +/- 0.52) and pachytene (25.8 +/- 0.96 to 5.35 +/- 0.26) spermatocytes and complete absence of any spermatids after the treatment. By contrast, round stage 7 and elongated spermatids were observed in many tubules of the testis in the age-matched control rats. At the end of GnRH antagonist treatment, the blood levels of LH were undetectable, while testosterone and FSH were decreased to 12 and 44% of the controls, respectively. Supplementation of either FSH (ovine FSH 20 micrograms/rat day-1) or testosterone (30 micrograms/rat day-1) enhanced the testicular weight (68%) and the circulatory levels of these hormones, but failed to support quantitatively normal spermatogenesis, which was, however, qualitatively improved. The number of maturing spermatids were comparatively higher in the testosterone-supplemented group that in the FSH-administered group. The latter group had otherwise the highest number of degenerating germ cells per tubule (mean 4.8 +/- 0.1). Testicular weight and stage-specific germ cell counts were restored to normalcy only in rats supplemented with both FSH and testosterone, the critical concentrations of which were important in the initial stages of spermatogenesis. Testosterone alone had a positive effect in terms of germ cell development, while FSH without testosterone was detrimental to the maturing germ cells.