ROLE OF GONADOTROPINS AND TESTOSTERONE ON INITIATION OF SPERMATOGENESIS IN THE IMMATURE RAT

Daily injections of specific antisera raised in rabbits against rat FSH or sheep LH were used to define the roles of gonadotropins and testosterone 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 adminstration of AS/FSH resulted in diminised 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 a 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 tubules diameter, fewer spermatocytes were noted and tubule lumena were absent. Testicular levels of testosterone (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. These observations suggest a requirement for FSH on some of the steps leading to the differentiation of type A spermatogonia into preleptotene spermatocytes and for the normal evolution of early spermiogenesis. They also confirm that testosterone is required for the completion 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.