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Abstract
The goal of this study was to examine the relative roles
of testosterone (T) and FSH in the proliferation and
differentiation of type Ap spermatogonia in the rhesus
monkey (Macaca mulatta). Twenty adult male monkeys
were treated with daily injections of a GnRH-receptor (R)
antagonist, acyline, to suppress endogeneous gonadotropin
secretion during an experiment comprising three phases.
Phase 1 established a chronic hypogonadotropic state
marked by a profound decrease in testicular size. During
phase 2, half of the monkeys were implanted with T-filled
capsules and the other half received control implants. T
treatment produced circulating T levels of approximately
15 ng/mL and normal testicular T content. At the end of
phase 2, monkeys were fitted with indwelling iv catheters
and housed in remote sampling cages for the final phase.
During phase 3, five monkeys from the T- and non T-treated
groups were stimulated with recombinant hFSH. The
remaining five monkeys from each group received an
infusion of vehicle. On the last day of FSH or vehicle
infusion, monkeys were bilaterally castrated after
receiving an iv bolus of bromodeoxyuridine (BrdU). BrdU
labeling of Ap spermatogonia was robust in the
hypogonadotropic group, and was uninfluenced by treatment
with T and FSH, either alone or in combination. In
contrast, both T and FSH stimulated spermatogonial
differentiation and this effect was amplified by combined
treatment. We conclude that: (1) marked Ap spermatogonial
proliferation occurs constitutively and in a gonadotropin
independent manner and, (2) differentiation of Ap into B
spermatogonia is absolutely gonadotropin dependent and may
be driven by either T or FSH.
Key words:
Testis
Follicle-stimulating hormone
Luteinizing hormone
Spermatogenesis
Testosterone
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