We hypothesize that the decrease in testicular GH-R concentration reflects the fact that GH-R are localized in one or several cell populations the proportion of which decreases rapidly when spermatogenesis develops. Only two studies have presented information on GH-R distribution in testis: in the rat, Lobie et al. reported a strong GH-R/GH-BP immunoreactivity in Leydig and Sertoli cells and moderate activity in most germ cell types, while in human testis, in situ hybridization revealed GH-R mRNA expression mainly in the seminiferous epithelium. buy prednisone
The data of Billard on the quantitative evolution of the various testicular cell types allow us to discuss various hypotheses concerning the distribution of GH-R in the rainbow trout testis. Decrease in testicular GH-R concentration did not correlate with the presence of these receptors in differentiating germ cells either because the proportion of these cells was stable (B spermatogonia) or because it increased (spermatocytes, spermatids) between stage II and V of spermatogenesis. Conversely, the localization of GH-R in the interstitial/peritubular tissue is compatible with our observations: the proportion of this tissue in trout testis undergoes a 4- to 5-fold reduction during spermatogenesis, similar to the 5-fold decrease in GH-R concentration we observed during that process. This is also in accordance with what we know of the GH effects on steroidogenic cells in vertebrates: GH increases the LH receptivity of mammalian testis and stimulates IGF-I mRNA content of cultured Leydig cells. GH also modifies the steroidogenic activity of mammals and fish testis, in vivo and in vitro (see Introduction and review ). To our knowledge, the search for GH binding sites in Leydig cell populations has not yet been undertaken.