HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -FSH MAINTENANCE OF CELLULAR VIABILITY DURING PUBERTAL SPERMATOGENESIS

Citation
Ld. Russell et al., HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -FSH MAINTENANCE OF CELLULAR VIABILITY DURING PUBERTAL SPERMATOGENESIS, Journal of andrology, 19(3), 1998, pp. 308-319
Citations number
45
Categorie Soggetti
Andrology
Journal title
ISSN journal
01963635
Volume
19
Issue
3
Year of publication
1998
Pages
308 - 319
Database
ISI
SICI code
0196-3635(1998)19:3<308:HOSITH>2.0.ZU;2-1
Abstract
The potential for follicle-stimulating hormone (FSH) to promote germ-c ell survival and the cellular sites of FSH action were studied using a gonadally maturing (pubertal), hypophysectomized (Hx) rat model in wh ich residual testosterone (T) activity was blocked by injections of an androgen-receptor antagonist, flutamide. Recombinant human FSH was gi ven to androgen-deprived and androgen-blocked male rats at 27 days of age to determine maintenance of individual germ-cell types at 35 days of age. Follicle-stimulating hormone significantly increased testis we ights and tubular diameters as compared with Hx and Hx-flutamide contr ols, although testis weights in FSH-treated animals were significantly lower than in pituitary-intact animals. Morphometric assays to determ ine ratios of germ cells to Sertoli cells and to determine the number of germ cells present per hour of development showed that the populati on of type A spermatogonia in the early stages of the cycle was not re sponsive to FSH. Follicle-stimulating hormone had a marked ability to maintain cell viability in the rapid, successive divisions that begin in the latter part of the cycle and that continue through the next cyc le (i.e., from type A, to A, and from intermediate spermatogonia to ty pe B spermatogonia to preleptotene spermatocytes to leptotene/zygotene spermatocytes to young pachytene spermatocytes). The data also sugges t T responsiveness of these cell types since the Hx-FSH-flutamide grou p showed lower cell viability at the aforementioned steps when compare d with the Hx-FSH group. Too few cell types were present at subsequent phases of spermatogenesis to allow a sensitive determination of FSH a ctivity in the maintenance of cell viability. The data show the potent ial of FSH in the absence or relative absence of T activity to maintai n cell viability. These data support the concept of overlapping and sy nergistic (or additive) effects of T and FSH in the immature rat and i dentify the cellular sites of FSH action.