REGULATION OF PROLACTIN SECRETION BY ADRENAL-STEROIDS IN ESTROGEN-TREATED OVARIECTOMIZED RATS - PARTICIPATION OF ENDOGENOUS OPIOID-PEPTIDES

The purpose of the present study was to determine whether glucocortico id inhibition of prolactin (PRL) release in oestrogen-treated ovariect omized (OVX) rats is mediated by endogenous opioid peptides (EOPs). Al l the animals were OVX and given oestradiol benzoate (OB, 20 mu g/rat, s.c.) 2 weeks later (day 0). On day 3 they received vehicle, mifepris tone (MIF, 10 mg/kg, s.c.) or hydrocortisone (HYD, 2 mg/rat, s.c.), in combination with the opioid antagonist naloxone (NAL, 2 mg/kg, i.p.) or vehicle. Serum PRL concentration was then measured by RIA at 13.00 and 18.00 hr, to include assessment of diurnal variation of PRL secret ion. At 13.00 hr either MIF or NAL alone increased PRL secretion with no additional effect when NAL was combined with MIF. HYD had no signif icant inhibitory effect, but NAL with HYD increased PRL secretion. At 18.00 hr serum PRL concentration was higher than at 13.00 hr, and not affected significantly by MIF or NAL alone, although PRL secretion was increased by treatment with both. HYD inhibited PRL secretion and thi s inhibition was prevented by NAL. In a second experiment to distingui sh antiglucocorticoid and antiprogesterone effects of MIF, we administ ered progesterone (2 mg/rat, s.c.) or a specific progesterone antiseru m. In contrast with MIF, the progesterone antibody had no effect on PR L secretion at 13.00 hr, nor on the stimulation by NAL, while progeste rone (unlike HYD) increased PRL secretion and NAL attenuated this resp onse; this was opposite to the effect of NAL with HYD. Similarly, al 1 8.00 hr the interaction of MIF and NAL was not explained by antagonism of progesterone. Together, these results indicate inhibition of PRL, by glucocorticoids but not progesterone, mediated in part by EOPs. At 18.00 hr endogenous glucocorticoids do not regulate oestrogen-stimulat ed PRL release, although HYD is inhibitory through EOPs. (C) 1997 Else vier Science Ltd.