Reproduction Abstracts

Introduction: Studies in primates indicated that AMH promotes preantral follicle growth, but inhibits antral follicle estradiol (E2) production in vitro. Thus, experiments were designed to investigate the role of AMH on primate follicular development in vivo during the spontaneous menstrual cycle.

Materials and methods: Hemi-ovariectomized, adult rhesus macaques (n=5) first received vehicle (control) treatment by intraovarian infusion from cycle day 1–4 to the midcycle E2 peak (follicular phase) via a catheter connected to an osmotic pump placed subcutaneously in the abdomen. After a recuperation cycle, the same ovary was infused with anti-human AMH antibody (AMH-Ab; 800 ng/h). Daily blood samples were collected for E2 and progesterone (P4) assays. Doppler 3D/4D ultrasonography was performed at the midcycle E2 peak to assess antral follicles.

Results and discussion: E2 peak levels tended to be higher during the AMH-Ab treatment compared with controls (251±68 vs 166±18 pg/ml). P4 levels were 2-3-fold higher (P<0.05) at the mid-to-late luteal phase following the AMH-Ab treatment compared with controls. Three of the five AMH-Ab-treated ovaries displayed multiple (n=2–9) medium-to-large (up to 8 mm) antral follicles at the midcycle E2 peak, whereas only one large (4-7 mm) antral follicle was observed during all control cycles. Thus, blocking endogenous AMH actions may promote macaque antral follicle growth during the follicular phase. Corpora lutea may develop from the multiple mature antral follicles and increase circulating P4 levels during the luteal phase. AMH may contribute to selection of the dominant follicle during the menstrual cycle by inhibiting antral follicle growth and maturation.

Support: NIH K12HD043488, Collins Medical Trust.