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 only by Sertoli cells, but postnatally, granulosa cells also produce this peptide growth/differentiation factor. We recently identified a candidate AMH type II receptor (AMHRII). In the present study, postnatal ovarian 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 granulosa 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 negative. Thecal and interstitial cells express no detectable AMH mRNA and little or no AMHRII mRNA. The colocalization of AMH and AMHRII mRNAs 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 AMHRII mRNA expression seems to persist somewhat longer than AMH mRNA. During the estrous cycle, no marked changes in the patterns of AMH and AMHRII 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 follicles. During the first weeks of postnatal development, AMH mRNA expression 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 localized to specific cell types. From postnatal day 15 onward, AMHRII mRNA expression becomes more restricted to the preantral and small antral follicles. Treatment of prepubertal rats with GnRH antagonist (Org 30276) and human recombinant FSH (Org 32489) or with GnRK antagonist and 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 play a role in the down-regulation of AMH and AMHRII mRNA expression in vivo when small antral follicles differentiate into large antral follicles. Furthermore, the FSH surge on the morning of estrus may inhibit AMH and AMHRII mRNA expression in preantral follicles. Autocrine action of AMH on granulosa cells of preantral and small antral follicles might result in the control of follicle maturation and/or play a role in follicle selection.