Pituitary gonadotropins regulate spermatogonial differentiation and proliferation in the rat‡

Abstract

The relative regulatory roles of the pituitary gonadotropins, luteinizing hormone and follicle stimulating hormone in the spermatogonial proliferation has been studied using specific antibodies against these hormones in the immature rats. Immunoneutralization of luteinizing hormone for 7 days resulted in significant reduction in tetraploid cells and total absence of haploid cells, while there was a relative increase in the diploid population. This was also accomopanied by a decrease in spermatogonial proliferation as indicated by a decrease in [ 3 H] thymidine incorporation into DNA by purified spermatogonia. Administration of follicle stimulating hormone a/s for 7 days also caused a significant decrease in the rate of spermatogonial proliferation. Withdrawal of follicle stimulating hormone led to a significant reduction in tetraploid and haploid cells. However interestingly, it failed to totally abolish the appearance of these cells. Administration of testosterone (3 mg/day/rat) for 2 days along with the gonadotropin a/s could partially reverse the effect on spermatogonial proliferation. It is concluded that (i) both luteinizing hormone and follicle stimulating hormone are involved in spermatogonial proliferation, (ii) lack of testosterone consequent of the neutralization of luteinizing hormone prevented the entry of spermatogonial cells into meiosis, (iii) testosterone may be involved in spermatogonia] proliferation providing a mitotic signal and (v) both follicle stimulating hormone and testosterone act synergistically and lack of any one of the hormones results in impairment of spermatogonial proliferation.

Insights into male germ cell apoptosis due to depletion of gonadotropins caused by GnRH antagonists

“…Similar results were also obtained with FSH receptor antibodies which caused the germ cell apoptosis (Dighe et al, unpublished observations) or reduction in the fertility [9]. Intriguingly, immunoneutralization of gonadotropins did not cause apoptosis of the spermatogonial population, but caused a decrease in their proliferation [10]. Thus, it appears that blocking of two gonadotropins differently affected different germ cells.…”

“…This recovery is probably due resurgence of spermatogenesis from the beginning with spermatogonial proliferation. Earlier data from the laboratory had clearly shown that immunoneutralization of gonadotropins does not cause apoptosis of spermatogonial population, but there was significant reduction in the rate of proliferation of these cells [10]. Restoration of spermatogenesis in hypo-gonadotropin patients by gonadotropin treatment is also probably due to initiation of spermatogenesis at the mitotic phase.…”

Ethnopharmacological Studies of <em>Tribulus Terrestris</em> (Linn). in Relation to its Aphrodisiac Properties

“…Since FSH and testosterone are proximally required by stertoll cell to support spermatogenesis (Carr and Griffin, 1992). They act synergistically, and influence the different steps of sperm cells, transformation during spermatogenesis (Shetty et al 1996). Depletion in the biosynthesis of these hormones due to external androgen could block spermatogenesis.…”

Effect of Various Chromatographic Fractions of Neem Seed Oil on Sperm Dynamics and Testicular Cell Population Dynamics of Male Albino Rats

“…It seems that the arrest of spermatogenesis is due to the reduced activity of Leydig cells (Kasturi et al, 1995). FSH plays a major role in transformation and maturation of round to elongated spermatid (Moudgal & Suresh, 1995;Shetty et al, 1996).…”