Increased oocyte degeneration and follicular atresia during the estrous cycle in anti-Müllerian hormone null mice.

Anti-Müllerian hormone (AMH) plays an important role in folliculogenesis. AMH null mice display an increased recruitment of primordial follicles. Nevertheless, these mice do not have proportionally more preovulatory follicles.

Anti-Müllerian hormone and its role in ovarian function.

Anti-Müllerian hormone (AMH) is expressed after birth in the ovary in the granulosa cells of healthy, small growing follicles. We have shown that AMH affects two important regulatory steps during folliculogenesis. At initial recruitment, AMH inhibits recruitment of primordial follicles into the growing pool, while at cyclic recruitment AMH lowers the FSH-sensitivity of follicles.

Regulation of ovarian function: the role of anti-Müllerian hormone.

Anti-Müllerian hormone (AMH), also known as Müllerian inhibiting substance, is a member of the transforming growth factor beta superfamily of growth and differentiation factors. In contrast to other members of the family, which exert a broad range of functions in multiple tissues, the principal function of AMH is to induce regression of the Müllerian ducts during male sex differentiation. However, the patterns of expression of AMH and its type II receptor in the postnatal ovary indicate that AMH may play an important role in ovarian folliculogenesis.

Anti-Müllerian hormone inhibits initiation of primordial follicle growth in the mouse ovary.

Recruitment of primordial follicles is essential for female fertility; however, the exact mechanisms regulating this process are largely unknown. Earlier studies using anti-Müllerian hormone (AMH)-deficient mice suggested that AMH is involved in the regulation of primordial follicle recruitment. We tested this hypothesis in a neonatal ovary culture system, in which ovaries from 2-d-old C57Bl/6J mice were cultured for 2 or 4 d in the absence or presence of AMH.