The role of inhibin and activin in the initiation of follicular development, growth, and atresia was examined. Human recombinant inhibin (1 μg) was unilaterally injected into the ovarian intrabursal space of 25-day-old rats. The contralateral ovary served as a control. Recruited growing follicles (350-500 μm) were observed 24 h after injection. The accumulation of follicles was greater in the inhibin-treated ovaries than in contralateral control ovaries. Moreover, the size distribution of the follicles was similar to the distribution of follicles recruited by systemic exogenous PMSG treatment. The effect of inhibin plus PMSG on follicular development was not different from that of PMSG treatment alone. Injection of human recombinant activin (1 μg) into the ovarian bursa caused follicular atresia. Activin therapy blocked the follicular development caused by PMSG treatment. The effect of inhibin and activin on follicular development was further characterized by measuring the incorporation of [3H]thymidine into dividing cells. Inhibin enhanced follicular thymidine incorporation, while activin decreased granulosa cell proliferation. Furthermore, receptors for inhibin-A (6.4 x 103receptors/cell) and activin-A (2.3 x 104receptors/cell) were identified on granulosa cells. The evidence suggests that inhibin and activin act in a paracrine manner to regulate follicular development, inhibin as a follicular growth signal and activin as an atretagenic signal.
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