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PARENT SESSION STEROIDOGENESIS AND HORMONE ACTION IN THE TESTIS Kent 7:30 AM-10:00 AM
(116) EXPRESSION OF ANTI-MULLERIAN HORMONE RECEPTOR-TYPE II IN CELLS OF LEYDIG CELL LINEAGE IN THE RAT TESTIS FROM BIRTH TO SEXUAL MATURITY.
Mendis-Handagama, S.M.L.Chamindrani1,2, Ariyaratne, H.B.Siril1, di Clemente, Nathalie2, Mrkonjich, LaDonna1, 1 Dept Comparative Medicine, Knoxville, TN2 Dept de Biologie, Montrouge, FR
ABSTRACT- It is suggested that the anti-Mullerian hormone (AMH) produced by the immature Sertoli cells is a negative regulator of the mesenchymal cell (MC) differentiation into Leydig cells in the postnatal testis. If AMH action on MC in the postnatal testis interstitium is direct, these MC should possess AMH receptors (AMHR). Therefore, the objective of the present study was to examine the presence of AMHR-type II in MC in the postnatal rat testis interstitium from birth to sexual maturity. Male Sprague Dawley rats of day 1, 5, 7-21, 28, 40, 60 and 90 were used. Their testes were fixed in Bouin's solution, processed and embedded in paraffin. The presence or absence of AMHR-type II in testicular MC and other cells in the Leydig cell lineage was tested by immunocytochemistry using Avidin-Biotin technique. The results revealed that MC were negative for AMHR-type II at all ages tested. A weak label was observed in fetal Leydig cells. Leydig cell progenitors and newly formed adult Leydig cells in 13-28 day rats also showed a positive label. The intensity of the label was much greater in adult Leydig cells at days 40, 60 and 90 compared to all other positive cells. Detection of AMHR-type II in Leydig cells and progenitors are in favor of the role of AMH in the steroidogenic function of these cells. Two alternatives could be suggested for the absence of AMHR-type II in MC of the present study. 1) The technique used is not sensitive enough for the detection of AMHR-type II or 2) it is unlikely that the negative regulatory effect of AMH on Leydig cell differentiation in the postnatal testis is achieved by a direct action of AMH on MC.
KEY WORDS: Leydig cell differentiation, Anti-Mullerian Hormone, Mesenchymal cells, Testis
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