Viguier-Martinez M C, Hochereau-de Reviers M T, Perreau C
Acta Endocrinol (Copenh). 1985 Aug;109(4):550-7. doi: 10.1530/acta.0.1090550.
Male rats treated prenatally with busulfan in order to render them aspermatogenic were treated between 23 and 38 days of age either with testosterone, or flutamide. In such aspermatogenic rats, testosterone supplementation stimulated the growth of accessory sex organs, markedly decreased the secretion of gonadotrophins (by 61% for LH and 83% for FSH), decreased testicular weight (-60%) as well as all parameters relating to testicular histology. Flutamide treatment decreased the weight of accessory sex organs, stimulated the secretion of both LH (+200%) and FSH (+63%) by inhibition of the negative feedback of testosterone; endogenous testosterone secretion was increased by 363%. Testicular weight was increased by 44% and the total volume and the cytoplasmic and nuclear area of Leydig cells were increased by 254 and 28%, respectively, but their number per testis was unchanged. The number of Sertoli cells per testis was increased by 49%, but their nuclear area was not modified. In aspermatogenic prepubertal rats, the large increase in plasma FSH demonstrated that FSH release was partly under the control of inhibin, secreted by Sertoli cells when germinal cells were present. Nevertheless, FSH levels after testosterone (inhibition) or flutamide treatment (stimulation) clearly demonstrated that, in the growing rat, FSH secretion is also partly dependent on the negative feedback of testosterone. In the absence of germ cells, FSH was able to re-initiate Sertoli cells mitoses, but not their functional activity. LH secretion was solely controlled by the negative feedback of androgens and, even in the absence of germinal cells, Leydig cells were able to respond to LH stimulation by an increase in testosterone secretion.
为使雄性大鼠无精子生成能力，在其出生前用白消安进行处理，然后在23至38日龄时分别用睾酮或氟他胺对其进行处理。在这种无精子生成的大鼠中，补充睾酮刺激了附属生殖器官的生长，显著降低了促性腺激素的分泌（促黄体生成素降低61%，促卵泡生成素降低83%），降低了睾丸重量（-60%）以及与睾丸组织学相关的所有参数。氟他胺处理降低了附属生殖器官的重量，通过抑制睾酮的负反馈刺激了促黄体生成素（+200%）和促卵泡生成素（+63%）的分泌；内源性睾酮分泌增加了363%。睾丸重量增加了44%，睾丸间质细胞的总体积、细胞质和细胞核面积分别增加了254%和28%，但其每只睾丸的数量未变。每只睾丸的支持细胞数量增加了49%，但其细胞核面积未改变。在青春期前无精子生成的大鼠中，血浆促卵泡生成素的大幅增加表明，促卵泡生成素的释放部分受抑制素控制，当有生殖细胞时由支持细胞分泌。然而，睾酮（抑制）或氟他胺处理（刺激）后的促卵泡生成素水平清楚地表明，在生长中的大鼠中，促卵泡生成素的分泌也部分依赖于睾酮的负反馈。在没有生殖细胞的情况下，促卵泡生成素能够重新启动支持细胞的有丝分裂，但不能启动其功能活动。促黄体生成素的分泌仅受雄激素负反馈的控制，即使没有生殖细胞，睾丸间质细胞也能够通过增加睾酮分泌来响应促黄体生成素的刺激。
