<Li> In males, FSH induces Sertoli cells to secrete androgen - binding proteins (ABPs), regulated by inhibin's negative feedback mechanism on the anterior pituitary . Specifically, activation of Sertoli cells by FSH sustains spermatogenesis and stimulates inhibin B secretion . </Li> <Li> In females, FSH initiates follicular growth, specifically affecting granulosa cells . With the concomitant rise in inhibin B, FSH levels then decline in the late follicular phase . This seems to be critical in selecting only the most advanced follicle to proceed to ovulation . At the end of the luteal phase, there is a slight rise in FSH that seems to be of importance to start the next ovulatory cycle . </Li> <P> Control of FSH release from the pituitary gland is unknown . Low frequency gonadotropin - releasing hormone (GnRH) pulses increase FSH mRNA levels in the rat, but is not directly correlated with an increase in circulating FSH . GnRH has been shown to play an important role in the secretion of FSH, with hypothalamic - pituitary disconnection leading to a cessation of FSH . GnRH administration leads to a return of FSH secretion . FSH is subject to oestrogen feed - back from the gonads via the hypothalamic pituitary gonadal axis . </P> <P> FSH stimulates the growth and recruitment of immature ovarian follicles in the ovary . In early (small) antral follicles, FSH is the major survival factor that rescues the small antral follicles (2--5 mm in diameter for humans) from apoptosis (programmed death of the somatic cells of the follicle and oocyte). In the luteal - follicle phase transition period the serum levels of progesterone and estrogen (primarily estradiol) decrease and no longer suppress the release of FSH, consequently FSH peaks at about day three (day one is the first day of menstrual flow). The cohort of small antral follicles is normally sufficient in number to produce enough Inhibin B to lower FSH serum levels . </P>

The period of time when cessation of fertility and hormone production has diminished is called