Effect of hormones on the Salientian spermatogenesis in vivo and in vitro

Abstract

In most of the tropical Salientia, the spermatogenic cycle is uninterrupted and is of the continuous type. With respect to spermatogenic rhythm, temperate frogs and toads are discontinuous since spermatogenesis ceases during the winter season. In a third group of anurans, a partial cessation of spermatogenesis is observed during unfavorable seasons. Hypophysectomy causes regression of the spermatogenetic elements which can be maintained either by injections of crude pituitary extract, by adenohypophyseal implants, or by administration of exogenous gonadotropin. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) administered separately can maintain the spermatogenetic cell nest and interstitium, repectively. LH alone, on the other hand, is detrimental to the spermatogenetic cells, but the inhibition is ameliorated by the administration of combined (FSH + LH) exogenous gonadotropin in different species of Salientia. Moreover, it appears that in Bufo melanostictus, Rana tigrina, and Rana pipiens the effect of FSH on the spermatogenetic cell nests is slightly improved in the presence of LH. Action of exogenous testosterone on the spermatogenesis of Bufo melanostictus, Rana tigrina, Rana hexadactyla, Rana pipiens, and Rana temporaria has also been studied. Testosterone appears to cause inhibition of the divisions of the spermatogonia. It has no effect on the development of the spermatocytes or spermatids, and it may even slightly accelerate the process. Furthermore, in some experiments with hypophysectomized Rana pipiens treated with exogenous testosterone and combined dose of gonadotropins, it was clear that, besides acting through the hypothalamohypophyseal axis, this steroid also had a direct inhibitory effect on the testicular germinal epithelium. Hormonal effects on the spermatogenesis of Rana pipiens have also been studied in vitro by an organ culture method. The combinations, FSH + LH, and FSH + LH + insulin + testosterone, resulted in almost complete testicular maintenance in vitro, and, in some circumstances, even stimulation of spermatogenesis occurred. However, in no case were secondary spermatocytes maintained in these organ cultures, and spermatogenesis could be stimulated only through the first meiotic division. Testosterone, previously demonstrated to inhibit spermatogenesis in vivo at the secondary spermatogonial level, exerted no such inhibitory action in vitro. Seasonal variations in the sensitivity of the testis to hormones and other conditions in vitro have also been noted.