REINITIATION OF SPERMATOGONIAL MITOTIC DIFFERENTIATION IN INACTIVE OLD BDF1 MOUSE SEMINIFEROUS TUBULES TRANSPLANTED TO W W-V MOUSE TESTIS/

Citation
K. Tanemura et al., REINITIATION OF SPERMATOGONIAL MITOTIC DIFFERENTIATION IN INACTIVE OLD BDF1 MOUSE SEMINIFEROUS TUBULES TRANSPLANTED TO W W-V MOUSE TESTIS/, Biology of reproduction, 55(6), 1996, pp. 1237-1242
Citations number
37
Categorie Soggetti
Reproductive Biology
Journal title
ISSN journal
00063363
Volume
55
Issue
6
Year of publication
1996
Pages
1237 - 1242
Database
ISI
SICI code
0006-3363(1996)55:6<1237:ROSMDI>2.0.ZU;2-#
Abstract
The seminiferous epithelia of old mice (33 mo of age) are composed of spermatogonia and Sertoli cells. Histochemical examination using the a nti-c-kit monoclonal antibody demonstrated that the number of differen tiating type A spermatogonia decreases with age. To elucidate the diff erential activity of old mouse spermatogonia, we transplanted extremel y thin seminiferous epithelia of old BDF, mice into W/W-v mouse testes and examined whether or not they could reinitiate differentiation. Ar tificially cryptorchid mice were used as the control. At 2 wk after tr ansplantation, spermatocytes and round spermatids were detected in tra nsplanted seminiferous tubules of the control, whereas the most advanc ed spermatogenic cells in those of old mice were spermatocytes. At 4 w k after transplantation, although elongated spermatids were detected i n transplanted tubules of the control, haploid cells (spermatids) were still undetectable in those derived from old mice. Thus, meiosis was never restored, although spermatogonia of old mice can reinitiate diff erentiation into spermatocytes under suitable testicular conditions. S ince it has been reported in several mammalian species that age-relate d changes in the testicular microenvironment lead to the gerontal cess ation of spermatogenesis, the present results suggest that both a defe ctive extratubular environment and a defective intratubular environmen t may cause the cessation of spermatogenesis in old BDF1 mice.