ANTI-MULLERIAN HORMONE AND ANTI-MULLERIAN HORMONE TYPE-II RECEPTOR MESSENGER-RIBONUCLEIC-ACID EXPRESSION IN RAT OVARIES DURING POSTNATAL-DEVELOPMENT, THE ESTROUS-CYCLE, AND GONADOTROPIN-INDUCED FOLLICLE GROWTH

During fetal development, anti-mullerian hormone (AMH) is produced onl y by Sertoli cells, but postnatally, granulosa cells also produce this peptide growth/differentiation factor. We recently identified a candi date AMH type II receptor (AMHRII). In the present study, postnatal ov arian AMH and AMHRII messenger RNA (mRNA) expression was studied by in situ hybridization and ribonuclease protection. In ovaries hom adult rats, AMH and AMHRII mRNAs were found to be mainly expressed in granul osa cells from preantral and small antral follicles. Corpora lutea and large antral follicles express Little or no AMH and AMHRII mRNA, and primordial follicles and oocytes appeared to be AMH and ABHRII mRNA ne gative. Thecal and interstitial cells express no detectable AMH mRNA a nd little or no AMHRII mRNA. The colocalization of AMH and AMHRII mRNA s in granulosa cells of specific follicle types suggests that actions of AMH via AMHRII are autocrine in nature. There is a decreased level of AMH and AMHRII mRNA expression when follicles become atretic. Both mRNA species are eventually lost from atretic follicles, although AMHR II mRNA expression seems to persist somewhat longer than AMH mRNA. Dur ing the estrous cycle, no marked changes in the patterns of AMH and AM HRII mRNA expression were detected, except at estrus, when expression of both mRNA species in preantral follicles was decreased compared to that an the other days of the cycle. On postnatal day 5, total ovarian AMH mRNA expression is low and is located in small preantral follicle s. During the first weeks of postnatal development, AMH mRNA expressio n in preantral follicles increases, and the later formed small antral follicles also express AMH mRNA. In contrast, AMHRII mRNA is expressed on postnatal day 5 at a higher level than AMK mRNA, but cannot be loc alized to specific cell types. From postnatal day 15 onward, AMHRII mR NA expression becomes more restricted to the preantral and small antra l follicles. Treatment of prepubertal rats with GnRH antagonist (Org 3 0276) and human recombinant FSH (Org 32489) or with GnRK antagonist an d estradiol benzoate resulted in follicle growth and inhibition of AMH and AMHRII mRNA expression in some, but not all, preantral and small antral follicles. These results indicate that FSH and estrogens may pl ay a role in the down-regulation of AMH and AMHRII mRNA expression in vivo when small antral follicles differentiate into large antral folli cles. Furthermore, the FSH surge on the morning of estrus may inhibit AMH and AMHRII mRNA expression in preantral follicles. Autocrine actio n of AMH on granulosa cells of preantral and small antral follicles mi ght result in the control of follicle maturation and/or play a role in follicle selection.