Hormone sensitivity of germ cells in stage XIV and in stage I of the rat spermatogenic cycle

Abstract

Previous data have been inconclusive with respect to whether the meiotic degenerations that occur in stage XIV of the spermatogenic cycle are increased after hypophysectomy. Meiotic cell degenerations in Stage XIV and early Stage I of the spermatogenic cycle were enumerated to determine if the advanced generation of meiotic cells were influenced by hormonal deprivation subsequent to hypophysectomy and, if so, could cellular degenerations be prevented by supplementation with either testosterone or recombinant FSH during the period of hypophysectomy. The animals utilized were either pituitary-intact rats or rats hypophysectomized for 3 or 10 days. Hormone supplementation began at day 3 post-hypophysectomy and continued until day 10 at which time all animals were sacrificed. The numbers of degenerating meiotic figures (metaphase to telophase of the first and second meiotic division) as expressed per Sertoli cell nucleus or nucleolus were not increased significantly 10 days after hypophysectomy as compared with animals hypophysectomized for 3 days or with pituitary-intact controls. Exogenously administered testosterone and FSH had no effect on the numbers of degenerating meiotic germ cells in hypophysectomized animals. These data indicate that stage XIV metaphase to telophase spermatocytes are not hormone sensitive. However, it was determined that there were new cell types degenerating at Stage XIV and I of the spermatogenic cycle. These were interphase secondary spermatocytes and step 1 spermatids and were seen in stages XIV and I, respectively. These cell degenerations were found in low numbers in Stage XIV and I in either FSH-treated or testosterone-treated rats, suggesting their hormone sensitivity. Thus it is possible that Stages XIV and I are hormone sensitive stages. Since the progenitors of these cells passed through Stage VII during a period of low hormonal levels, it is also possible that they degenerate in Stage XIV as the result of earlier hormone inadequacy.