One of the most interesting findings from this study is that activin A and inhibin A had the same effect and did not antagonize each other in oocyte maturation. In agreement with these findings, an earlier study on goldfish pituitary also found that both activin and inhibin stimulated gonadotropin-II release. Interestingly, while most studies in mammals have shown that activin and inhibin have opposite functions and that inhibin is a functional antagonist of activin, Alak et al. reported that activin A and inhibin A both enhanced oocyte maturation in rhesus monkeys. Since activin A and inhibin A had additive effects on monkey oocyte maturation, it was suggested that they might act at different levels and/or by different mechanisms. However, no additive effects of activin A and inhibin A on oocyte maturation were observed in our study, suggesting a similar mechanism of action for both activin A and inhibin A. In mammals, inhibin has an affinity for activin receptors and has been shown to block activin action by binding to activin type II receptors and preventing the association between type I and type II. Whether or not inhibin can bind to activin receptors in fish is not known.
FS are known to be binding proteins for activins and inhibins. FS-288 has been shown to neutralize activin functions in many tissues and cells. In the present study, the effect of activin A and inhibin A was completely neutralized by FS-288, supporting the specificity of activin A and inhibin A action. Furthermore, FS-288 also suppressed gonadotropin- and MIH-induced final oocyte maturation. These findings suggest that activins and/or inhibins are autocrine/paracrine regulators that mediate, at least in part, the action of gonadotropin and MIH in the induction of final oocyte maturation. These results are consistent with the findings of Pang and Ge.