FOLLICLE-STIMULATING-HORMONE, HUMAN CHORIONIC-GONADOTROPIN, AND PROLACTIN RECEPTORS IN HAMSTER CORPORA-LUTEA OR DISPERSED LUTEAL CELLS DURING PREGNANCY

In vitro progesterone (P-4) production by hamster luteal cells is stimulated throughout pregnancy by FSH and LH. Prolactin (PRL) by itself, however, increases P-4 synthesis only on Day 12; on Day 4, FSH+LH+PRL. induces optimal P-4 secretion [Biol Reprod 1994; 51:43-49]. In light of these findings, in this study we investigated FSH, hCG, and PRL receptors in hamster CL or dispersed luteal cells on Days 4, 8, and 12 of pregnancy. Scatchard analysis of hamster CL on Days 4 and 8 showed considerably more unoccupied hCG receptors than FSH receptors: on Day 4, there was 9.5 fmol/mg protein for FSH binding sites vs. 1741 fmol/mg protein for hCG binding. Moreover, the binding affinity of hCG was greater than for FSH: the Day 4 K-d was 0.136 nM for hCG vs. 0.308 for FSH. Similar differences were observed on Day 8. Dispersed luteal cells (large + small cells) were incubated for 24 h with or without 10 ng of ovine FSH, LH, and PRL or human recombinant FSH (r-hFSH), alone or in different combinations. The cells were then washed and incubated for 4 h with iodinated hCG, FSH, or PRL. with or without 100-fold excess of unlabeled hormones. The number of binding sites per 200 000 luteal cells did not change appreciably for FSH and hCG on Days 4 and 12 of pregnancy, whereas PRL binding sites significantly increased on Day 12. Incubation for 24 h with PRL or FSH or FSH+PRL statistically increased hCG binding sites on Days 4 and 12; LH alone did not increase hCG binding over control values, nor did FSH+LH, PRL+LH, or FSH+LH+PRL up-regulate hCG receptors beyond the effects of FSH, PRL, or FSH+PRL. The presence of FSH, PRL, and LH receptors on Days 4 and 12 of pregnancy supports the significant in vitro luteotropic effects of these hormones. However, the optimal in vitro synthesis of P-4 by FSH+LH+PRL cannot be explained by a synergistic increase in hCG binding sites and most likely results from an increase of cAMP [Biol Reprod 1994; 51:472-479] or other second messenger systems.