ROLES OF FSH AND TESTOSTERONE IN THE INITIATION OF SPERMATOGENESIS INPREPUBERTAL RATS MEDICALLY HYPOPHYSECTOMIZED BY A GNRH ANTAGONIST

Experimentally induced medical hypophysectomy in prepubertal rats thro ugh treatment of GnRH antagonist for 3 weeks, initiated on the 20th da y of age, markedly decreased testicular weight by 85% of that of the c ontrols. Quantitative assessment of spermatogenesis in testicular semi thin preparations revealed a significant reduction in the numbers of p releptotene (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 spermat ids after the treatment. By contrast, round stage 7 and elongated sper matids 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 F SH (ovine FSH 20 mug/rat day-1) or testosterone (30 mug/rat day-1) enh anced 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 sp ermatids were comparatively higher in the testosterone-supplemented gr oup 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 res tored to normalcy only in rats supplemented with both FSH and testoste rone, the critical concentrations of which were important in the initi al 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.