ANDROGEN RECEPTOR DISTRIBUTION IN RAT TESTIS - NEW IMPLICATIONS FOR ANDROGEN REGULATION OF SPERMATOGENESIS

Citation
W. Vornberger et al., ANDROGEN RECEPTOR DISTRIBUTION IN RAT TESTIS - NEW IMPLICATIONS FOR ANDROGEN REGULATION OF SPERMATOGENESIS, Endocrinology, 134(5), 1994, pp. 2307-2316
Citations number
62
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
134
Issue
5
Year of publication
1994
Pages
2307 - 2316
Database
ISI
SICI code
0013-7227(1994)134:5<2307:ARDIRT>2.0.ZU;2-F
Abstract
The distribution of the androgen receptor (AR) in the adult rat testis was determined by biotin-streptavidin immunoperoxidase, employing tis sue embedded in polyester wax which preserves antigenicity without com promising tissue preservation. The antibody probe used, which has been characterized previously, was an affinity purified, rabbit polyclonal antibody raised to the amino terminus peptide of the rat AR. Within t he interstitial compartment, AR immunostaining was detected in some Le ydig cells and all smooth muscle cells forming the walls of blood vess els, but endothelial cells of blood vessels were negative. Furthermore , in those Leydig cells that were clearly identified as exhibiting AR immunostaining, the intensity of the reaction varied. In the seminifer ous tubules AR immunostaining was observed in all peritubular myoid ce ll nuclei, but not in the distal layer of lymphatic endothelial cells. In Sertoli cells, nuclear AR immunostaining was stage. specific. Mode rate AR immunostaining first became evident at late stage IV or early stage V of the cycle, reached a robust peak at stages VII-VIII, and th en disappeared completely. Specific AR immunostaining was also discern ed in the nuclei of stage XI elongated spermatids, the spermatids in w hich nuclear elongation is apparent but chromatin condensation has not yet begun. Next, with onset of chromatin condensation, nuclear AR imm unostaining in elongated spermatids was not discerned concomitant with its detection in the cytoplasm of the germ cells. These results are i nterpreted in the following manner: 1) The presence of AR in Leydig ce lls is consistent with the hypothesis that androgens modify Leydig cel l activity in an autocrine fashion. Further, that not all Leydig cells exhibited AR immunostaining at steady state suggests a differential, functional activity of these cells within the population. 2) The inten se AR immunostaining of smooth muscle cells present in the interstitiu m indicates that these cells are targets for androgens. 3) AR immunore activity in both Sertoli and peritubular myoid cells suggests their in volvement in the androgenic control of spermatogenesis. The stage spec ific AR immunoreactivity in Sertoli cells, however, may be more indica tive of a specific androgen response during these stages, whereas peri tubular cells may participate in the tonal maintenance of spermatogene sis. 4) The specific presence of AR in step 11 elongated spermatids ma y suggest that androgens can act directly on germ cells to regulate sp ermatogenesis.