The Role of Gonadotropins and Testosterone on Initiation of Spermatogenesis in the Immature Rat1

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Abstract
Daily injections of specific antisera raised in rabbits against rat FSH [follitropin] or sheep LH [lutropin] were used to define the roles of gonadotropins and testosterone [T] on the initiation of spermatogenesis in the rat. Groups of immature Sprague-Dawley rats were treated from the day of birth up to 32 days of age according to 1 of the following schedules: control group injected with normal rabbit serum (NRS); antiserum to FSH (AS/FSH); antiserum to LH (AS/LH) or antiserum to LH plus testosterone propionate (AS/LH + TP). All animals were killed at 33 days of age. In control rats, spermatogenesis proceeded to the early elongation phase of spermatid development. The administration of AS/FSH resulted in diminished diameter of the seminiferous tubules, but tubule lumena were usually present. Quantitation of germ cells demonstrated normal numbers of type A spermatogonia and a reduction of preleptotene spermatocytes and steps 7-8 spermatids. The AS/LH treated rats showed a severe reduction of seminiferous tubule diameter and an arrest of spermatogenesis prior to completion of meiosis. Some tubules had a small lumen. The AS/LH + TP treated group showed a more advanced testicular regression compared with the AS/LH treated group. There was an extreme diminution of tubule diameter, fewer spermatocytes were noted and tubule lumena were absent. Testicular levels of T and dihydrotestosterone (DHT) were determined by radioimmunoassay and the ratio of T to DHT was: controls, 1:2.5; AS/FSH, 1:2.0; AS/LH, 1:0.5; AS/LH + TP, 1:0.3. FSH may be required for some of the steps leading to the differentiation of type A spermatogonia into preleptotene spermatocytes and for the normal evolution of early spermiogenesis. T is evidently required for the completion of of meiosis. The failure of TP to reverse the effects of AS/LH administration could be attributed to the possibly severe FSH inhibition induced by the high T plasma levels or to the alterations of the T:DHT ratio.