Human chorionic gonadotropin (hCG) fails to stimulate gonocyte differentiation in newborn mouse testes in organ culture.

The primitive germ cells within the postnatal testis differentiate through several steps to form primary spermatocytes, which are required for postpubertal spermatogenesis. It is postulated that this germ cell development is controlled by the hypothalamic-pituitary-gonadal axis. To study the effect of human chorionic gonadotropin (hCG) on postnatal testicular germ cell differentiation, especially on gonocytes, newborn mouse testes (n = 75) were cultured for 7 days in vitro. The synthetic serum-free medium contained either hCG or exogenous human recombinant müllerian inhibiting substance (MIS) plus transferrin, insulin and retinoic acid (TIRA). Fetal calf serum 10% (FCS) was used for control medium. Thirty-eight newborn mouse testes were cultured with hCG (0.1 to 2.0 IU/ml). The percentages of differentiated type-A spermatogonia were not significantly increased compared with synthetic medium alone (NS, p > 0.05), but were only 5 to 7% (p < 0.001) of that of serum-containing medium. By contrast, normal transformation from gonocytes to type-A spermatogonia occurred in newborn mouse testes (n = 10) cultured with serum-free medium containing exogenous MIS. The percentage of differentiated type-A spermatogonia was approximately 77% (NS, p > 0.05) of those seen in serum-containing medium. These findings demonstrate that the transformation of gonocytes to type-A spermatogonia is regulated by MIS, rather than hCG. As early germ cell transformation is deficient in boys with cryptorchidism, the role of hCG in the treatment of infertility associated with undescended testes should be reevaluated.