During the last year, we have extended our previous studies on the role of inhibin in regulating gonadotropin secretion by examining the role of inhibin in mediating the priming action of LHRH on the pituitary. Recent evidence in rats, primates and humans suggests than an ovarian substance is responsible for maintaining the pituitary in a state of low responsiveness to LHRH that must be overcome by LHRH """"""""priming"""""""". To determine the involvement of inhibin in this phenomenon, endogenous inhibin was immunoneutralized in vivo and responsiveness of the pituitaries to LHRH examined in vitro. The results from these studies revealed that endogenous inhibin is responsible for maintaining the pituitary in a low responsive state to LHRH during the follicular phase of the female estrous cycle by antagonizing the action of estradiol to increase pituitary sensitivity to LHRH, both directly by opposing estradiol action at the level of the pituitary and indirectly by suppressing the secretion of estradiol from the ovary. Inhibin may thus act to prevent premature and improperly timed surges of the gonadotropins and, therefore, has important implications in regulating ovulation and in vitro fertilization techniques. In other studies, the role of inhibin in regulating the suppression of gonadotropin secretion, during the transition of the male hamster from a long to short photoperiod, was examined as a possible model for studying gonadotropin regulation during puberty. We previously demonstrated that inhibin suppresses gonadotropin secretion prior to but not after puberty in the male rat. It was demonstrated that a reinstatement of the prepubertal-like suppressive inhibin tone may be the cause of the return of the hamster to a prepubertal-like state during the transition from long to short light cycle. These observations reveal a possible mechanism for the phenomenon of short photoperiod reproductive quiescence. In addition, the hamster has been demonstrated to be an important model for studying the hormonal transitions of puberty. The results from these and ongoing studies are dissecting the mechanisms and gonads interact to control reproductive function.
