Inhibitory effects of exogenously induced hyperprolactinemia on the endogenous cyclic release of luteinizing hormone and prolactin in the estrogen-primed ovariectomized rat.

The inhibitory effects of acute hyperprolactinemia on the cyclic release of LH and PRL were examined in the ovariectomized estradiol-treated rat. In Exp 1, animals were ovariectomized (day 0) and received sc injections of ovine (o) PRL (4 mg/kg BW) or vehicle beginning at 0900 h on day 4, 6, or 7 postovariectomy and continuing every 8 h until 0900 h on day 9. All animals were given Silastic capsules containing estradiol (E2) on day 7, were cannulated via the external jugular vein on day 8, and were bled at 0900 and 1030 h and at hourly intervals between 1200-1800 h on day 9. No effect of oPRL treatment on the cyclic release of LH was seen in 1-week ovariectomized rats regardless of the duration of PRL treatment. The endogenous rat PRL surge was attenuated by treatment with oPRL. In Exp 2, animals were ovariectomized (day 0) and, beginning on day 11 or 14 postovariectomy, received sc injections of oPRL or vehicle every 8 h until 0900 h on day 16. On day 14, animals received Silastic E2 capsules. The following day (day 15), the external jugular vein was cannulated, and at 1800 h, E2 capsules were removed from half of the rats. On day 16, rats were bled at the times outlined in Exp 1. When E2 levels were maintained by the continuous presence of an E2 capsule, hyperprolactinemia did not suppress the cyclic release of LH and only attenuated or shifted the timing of the rat PRL surge. In marked contrast, when E2 stimulation was discontinuous, oPRL abolished the steroid-induced LH surge in all animals treated with oPRL beginning on day 11 and in 57% of the animals treated beginning on day 14. Treatment with oPRL abolished the endogenous PRL surge in all animals regardless of the duration of PRL exposure. In conclusion, oPRL-induced hyperprolactinemia can inhibit E2-induced LH and PRL surges in long term ovariectomized rats under conditions of discontinuous E2 exposure. In contrast, when estrogen levels are maintained, hyperprolactinemia had no effect on the LH surge and only attenuated or shifted the timing of the endogenous PRL surge. Thus, the long term ovariectomized rat receiving discontinuous E2 provides a model that is particularly suited for the study of the possible neural mechanisms by which PRL inhibits cyclic release of LH.