A. Ganguly et al., ROLES OF FSH AND TESTOSTERONE IN THE INITIATION OF SPERMATOGENESIS INPREPUBERTAL RATS MEDICALLY HYPOPHYSECTOMIZED BY A GNRH ANTAGONIST, Archives of andrology, 32(2), 1994, pp. 111-120
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.