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Biology of Reproduction, Vol 21, 241-249, Copyright © 1979 by Society for the Study of Reproduction
1 Department of Anatomy,
and
Laboratory of Human Reproduction and Reproductive Biology,
Harvard Medical School,
Boston, Massachusetts 02115 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 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 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.
Note:
ACKNOWLEDGMENTS
The authors thank Dr. D. W. Fawcett for his advise
and critical reading of the manuscript. The skillful
technical help of Miss B. Rup is acknowledged. The
purified ovine LH was kindly provided by Dr. H.
Papkoff.
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