Figure 1.

Control of spermatogenesis. (A) Hormonal control. Gonadotropin-releasing hormone (GnRH) produced by the hypothalamus stimulates, by activating its receptors (GnRHR), the synthesis and release of the gonadotropins LH and FSH in the anterior pituitary gland. LH induces the proliferation and maturation of interstitial Leydig cells which will secrete T. FSH acts on the Sertoli cells (SC) of the seminiferous tubules by stimulating the production of signaling molecules and metabolites necessary for spermatogenesis. In conjunction with T and FSH the Sertoli cells indirectly stimulate the proliferation and maturation of germ cells in the seminiferous tubules from which mature sperm are released to the seminiferous tubular fluid and transported to the epididymis for storage and final maturation. (B) The three waves of Leydig cell proliferation in humans. Each of them is characterized by the production of T. The first wave is antenatal, occurring after 10 weeks of fetal life and is hCG-dependent. Fetal T secretion peaks at 14–15 weeks, and induces the differentiation of the internal genitalia and masculinization of the external genitalia. The other two waves of Leydig cell proliferation are postnatal, regulated by pituitary LH. At the end of the second month of life, in the postnatal period, the HPG axis is transiently activated. The increased secretion of LH and FSH causes the development of a second wave of Leydig cells, and the appearance of a peak of T at levels close in magnitude to those observed at puberty. This event, called “mini-puberty”, is short-lived, and its role is poorly understood. The third wave starts at puberty and lasts for the rest of a man’s life.