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Hormonal control of spermatogenesis.
172
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1967
Year
SpermatogenesisFertilityHormonal ControlReproductive BiologyFertilisationReproductive PhysiologyReproductive EndocrinologyGerm Cell DevelopmentPublic HealthInfertilityAndrologyGameteTestosterone PropionateMorphogenesisEndocrinologyHuman ReproductionDevelopmental BiologyPhysiologyMedicineReduction DivisionEstradiol BenzoateReproductive Hormone
The effect of estradiol benzoate (EB) testosterone propionate (TP) or pregnant mares serum gonadotropin (PMSG) administered singly or in combination on spermatogenesis was studied in rats. EB and TP treatment was initiated on the day of birth. Spermatogenesis progressed in EB-treated rats to a stage similar to that of 15-day-old untreated animals. However pachytene spermatocytes were unable to complete the reduction division and degenerated at diakinesis. Pituitary gonadotropic hormones and testosterone were not necessary for the progression of type A spermatogonia. Spermatogonic activity was inversely related to the duration of treatment with EB. TP administered at the pachytene stage of development to EB-treated animals resulted in a markedly increased testicular weight when compared with animals treated with EB only. Thus the reduction division of primary spermatocytes requires testosterone. Spermatogenesis proceeds up to Step 7 of spermiogenesis through the influence of TP; addition of PMSG completes spermiogenesis. Follicle-stimulating hormone is required for the completion of spermiogenesis. It is suggested that the dose of gonadotropins is of critical importance in the quantitative initiation and maintenance of spermatogenesis although the exact hormonal requirements for maintenance of normal spermatogenesis are unclear.