MAMMALIAN TESTIS 



341 



• fW-" 



12 



Fig. 5.20. Klicct oi Ti-siostcioiic on testis oi li\|M)pli\-,~(i lomi/i d lat //, testis of norm.al 

 rat, 30 days of age. 12, testis of 60-day-old rat li^popli^x ( tomizcd at 30 days of age. 13, 

 testis of 60-day-old rat hypophysectomized at 30 (la.\s of age and given 1000 /lig. testosterone 

 propionate daily for 30 days. (From D. J. Liidwig, Endocrinology, 46, 453, 1950.) 



However, larger doses generally have been 

 used in experiments on the maintenance of 

 spermatogenesis. These doses are far greater 

 than those necessary to maintain the acces- 

 sory sex organs of castrated animals. Tu- 

 bules can be maintained by much smaller 

 doses of testosterone. Dvoskin (1944) im- 

 planted pellets of testosterone intratesticu- 

 larly; approximately one-tenth of the 

 amount of testosterone needed by tlie par- 

 enteral route was effective by this route. 



The concept that testosterone maintains 

 spermatogenesis in hypophysectomized rats 

 was challenged by Simpson, Li and Evans 

 (1942, 1944) and by Simpson and Evans 

 (1946a, b). These investigators found that 

 gonadotrophins, including interstitial cell- 

 stimulating hormone (ICSH), maintained 

 spermatogenesis in hypophysectomized rats 

 at doses far lower than those needed to 



maintain the Leydig cells and the acces- 

 sories. The testes remained in the scrotum, 

 and motile sperm cells were produced. Inas- 

 much as testosterone propionate can main- 

 tain the tubules only at doses effective in 

 maintaining the accessories, it was doubted 

 that maintenance of spermatogenesis oc- 

 curred by way of the direct tubular action 

 of androgen. In addition to casting some 

 doubt on the accepted mechanism of the 

 spermatogenic action of androgen, this work 

 raised doubt concerning the dualistic con- 

 cept of gonadotrophic control of the testis. 

 Maintenance of the testis by ICSH after 

 hypoj^hysectomy suggests that one gonado- 

 trophic hormone may be sufficient to main- 

 tain testicular function in mammals. How- 

 ever, these findings may be interpreted 

 conventionally; i.e., that ICSH caused the 

 Leydig cells, even though they were not re- 



