In vitro approach to the control of spermatogonia proliferation in the trout.

When spermatogonia and primary spermatocytes (G(o) + CI), uncontaminated by somatic testicular cells, were prepared from trout testes at various maturation stages and cultured alone, basal tritiated thymidine (3H-Tdr) incorporation decreased throughout the reproductive cycle. It was unchanged by salmon gonadotropin (sGtH II), trout growth hormone (rhGH), testosterone, estradiol and 17 alpha, 20 beta-dihydroprogesterone. Conversely, it was dose-dependently stimulated by rhIGF-I, with a mean ED50 of 5.2 ng/ml and a mean maximum stimulation of 3.2-fold above control. When Go + CI were cultured either in the presence of Sertoli cells or in Sertoli cell-conditioned medium (SCCM), basal 3H-Tdr incorporation was always decreased when the Sertoli cells were from spermatogenetic testes, but it was stimulated when they were from testes which were to resume spermatogenesis soon. Whatever the origin of the Sertoli cells, they always partly inhibited IGF-I stimulation. When present during either the co-cultures or the preparation of SCCM, sGtH II and rtGH had no effect when Sertoli cells were from spermatogenetic testes. In conclusion, IGF-I is a direct efficient stimulator of the proliferation of trout male germ cells, the effect of which is partly counteracted by Sertoli cells. sGtH II, rtGH and the 3 tested steroids are not directly active. While sGtH II has no Sertoli cell-mediated activity, further investigation is necessary to clarify whether the other tested molecules have such an activity.