Hormonal Control of Pubertal Spermatogenesis

Abstract

The spermatogenic process of normal rats at 20, 32, and 44 days of age was characterized. Variations in numbers of degenerating and abnormal cells were noted during the cycle in most age groups, indicating a stage-related vulnerability of these cells. The most advanced cell types that were seen at a particular age were frequently abnormal or degenerating. When the numbers of viable cells available to degenerate were considered, the degeneration rate in normal pubertal animals was about 15, 10, and 2 times greater in 20-, 32-, and 44-day-old animals, respectively, than in 75-day-old animals. In 32-day-old rats, neither hypophysectomy nor hypophysectomy and subsequent hormone supplementation resulted in an alteration in the qualitative pattern of germ cell degeneration during the spermatogenic cycle compared with that in the normal animal; however, the treatments did alter the quantitative response of cellular degeneration. Three days posthypophysectomy there was a marked increase in the numbers of total degenerating germ cells. FSH (60 micrograms) given twice daily (as were all hormones) reduced the numbers of degenerating cells significantly, as did LH (13 micrograms). Low dose LH (0.3 micrograms), representing the approximate contaminating dose of LH in the 60-micrograms FSH preparation, and low dose FSH (30 micrograms) did not elicit a response significantly different from that to hypophysectomy alone. LH (13 micrograms) plus FSH (60 micrograms) reduced the levels of degenerating cells such that there was no significant difference from levels in intact 32-day-old rats. The data indicated, for the cell types studied, a lack of specificity of various hormones or hormone combinations in the survival of specific germ cell types. It emphasizes the importance of FSH in pubertal spermatogenesis as well as the synergistic actions of LH and FSH.

Testicular Activity of Mice Treated With MeOH Extract of Achyranthes aspera Leaves

“…It is evident that FSH stimulates the development of spermatogonia to spermatocytes and also maintains the spermatogenic process [38] and both FSH and LH/ICSH are necessary for meiosis and development of spermatids [39]. The androgens are necessary to induce meiosis, formation and development of spermatids in response to FSH [40].…”

Triiodothyronine modulates initiation of spermatogenesis in rats depending on treatment timing and blood level of the hormone

“…The germ cell types present on pnd 16 were identified on the basis of previously reported morphological characteristics (Russell and Frank, 1978;Russell et al, 1987). In rats, an adult rate of premeiotic spermatogenic progression was observed from day 15 onward whereas a much higher rate of progression of spermatogenesis was observed before this age (van Haaster and de Rooij, 1993).…”

“…There are both differentiating A spermatogonia that give rise to the first wave of spermatogenesis as well as spermatogonial stem cells de Rooij, 2001;de Rooij and Russell, 2000). Spermatogonial development finalizes on about pnd 10 with the first appearance of preleptotene spermatocytes Kula, 1977;Russell et al, 1987;van Haaster and de Rooij, 1993) while the differentiation of Sertoli cells finalizes on about pnd 16, together with cessation of their proliferation (Orth, 1982;Steinberger and Steinberger, 1971). The formation of junctions between Sertoli cells (StPierre et al, 2003;Vitale et al, 1973) is associated with the accretion of tubular lumen, reflecting fluid secretion by maturing Sertoli cells (Russell et al, 1989).…”

“…The initiation of spermatogenesis requires FSH, testosterone and estradiol action, (Almiron and Chemes, 1988;Kula et al, 2001;Russell et al, 1987;Walczak-Jedrzejowska et al, 2008).…”

Hepatocyte growth factor modulates in vitro survival and proliferation of germ cells during postnatal testis development

“…It has long been known that testosterone and follicle-stimulating hormone (FSH) regulate germ cell apoptosis, respectively inducing and preventing apoptosis of the germ cells (Madhwa Raj & Dym 1976, Russell et al 1987, Henriksen et al 1995.…”