A switch in Sertoli cell responsiveness to FSH may be responsible for robust onset of germ cell differentiation during prepubartal testicular maturation in rats

摘要

FSH receptor (FSH-R) is a G protein-coupled receptor, which, upon binding to FSH, gets activated and stimulates adenylyl cyclase (AC)-mediated production of cAMP. This second messenger activates a sequence of signaling events that elicit the biological actions of this gonadotropin (69). Although mice lacking FSH P-subunit (40) or FSH-R (1, 19) were reported to be fertile, these animals showed low sperm counts, smaller testicular size, and reduced litter size. In immature rats, FSH has been shown to regulate the survival, proliferation, and differentiation of spermatogonial cells (39, 45). Interestingly, FSH deprivation in rats minimizes the survival and differentiation of the Gc in 18 days of age but affects only Sc proliferation up to 9 days of age (46). The major action of FSH in spermatogenesis is therefore believed to induce Sc proliferation and to provide survival and differentiation signal to the developing Gc in rats. FSH is shown to stimulate the ERK-MAPK pathway in cultured Sc obtained from 5-day-old rats mainly to regulate Sc proliferation, whereas the PKA pathway is reported to dominate FSH-mediated action in Sc cultured from 19 days of age (12). Stem cell factor (SCF) and glial cell line-derived neurotrophic factor (GDNF) are the known putative downstream targets of FSH (65, 75) that are involved in the division, differentiation, and survival of repopulating sper-matogonia (47, 77). However, no study has yet been done to associate FSH-R activity and the expression of these genes in rat Sc during postnatal development,