Luteinizing hormone-dependent activity and luteinizing hormone-independentdifferentiation of rat fetal Leydig cells

Addition of 5 x 10(-2) U/ml recombinant luteinizing hormone (LH) to testes from fetuses at 16.5 day post conception (dpc) cultured for 5 days increase d the number of Leydig cells by 34% and the acute LH-stimulated testosteron e production by 600%. To determine whether these positive effects of LH in vitro are physiologically relevant in vivo, fetuses were decapitated on day s 16.5 pc (before the onset of LH expression in the hypophysis) or 18.5 pc (before the surge of LH in the fetal plasma) and removed at 21.5 dpc. The n umber of fetal Leydig cells per testis and the acute LH-stimulated testoste rone production by the testes ex vivo were unaltered by decapitation. Since , in all groups, the number of Leydig cells doubled between 16.5 and 18.5 d pc and between 18.5 and 21.5 dpc, these results suggest that neither the ap pearance of new fully differentiated fetal Leydig cells nor the maintenance of differentiated functions in existing fetal Leydig cells depend on LH du ring late fetal life, although this hormone is present in the plasma. Decap itation reduced the testosterone concentrations in the plasma (- 56%) and i n the testis in vivo (- 67%) and the basal testosterone secretion of the te stis ex vivo (- 70%). This suggests that LH is required to maintain the phy siological activity of the Leydig cell during late fetal life. However, the decrease of the in vivo testosterone production after decapitation was not sufficient to impair the growth of the Wolffian ducts and the lengtheninig of the anogenital distance. In conclusion, during late fetal life in the r at, Leydig cells are LH-independent for their functional differentiation an d LH-dependent for their activity. (C) 2001 Elsevier Science Ireland Ltd. A ll rights reserved.