These studies were conducted to determine the mechanisms by which prolactin (PRL) exerts its luteotropic effects on the mink corpus luteum (CL). Three experimental models were developed and utilized in these studies. In the first model, the ovaries from pregnant mink were collected at regular intervals throughout gestation, half the animals were treated with the dopamine agonist 2-bromo-$ alpha$-ergocryptine (bromocryptine), to suppress their endogenous PRL levels, and half were exposed to their endogenous PRL levels. The second model consisted of treating anestrous animals with exogenous gonadotropins to induce follicular development and ovulation, half the animals were then treated with PRL while the other half were left as untreated controls. In the third model, CL were collected from mink at several stages of mink gestation. The cells were enzymatically dispersed, placed in culture and incubated with different concentrations of PRL, luteinizing hormone (LH), follicle stimulating hormone (FSH) and (Bu)$ sb2$cAMP. Using these 3 models, the effects of PRL on P450 side chain cleavage (P450scc), 3$ beta$-hydroxysteroid dehydrogenase (3$ beta$-HSD), steroidogenic acute regulatory protein (StAR), luteinizing hormone receptor (LHr) and prolactin receptor (PRLr) mRNA were determined. Messenger RNA levels for P450scc did not vary significantly over the course of mink gestation and treatment of animals with bromocryptine did not alter the abundance. In the anestrous model, treatment of mink with PRL reduced P450scc mRNA levels below that of the untreated control, while treatment of cultured mink luteal cells with increasing concentrations of PRL had no effect on the abundance of P450scc mRNA. The abundance of 3$ beta$-HSD mRNA varied over the course of mink gestation. Levels were low during embryonic diapause, increased during CL reactivation and peaked during post-implantation gestation. Treatment of mink with bromocryptine prevented the pre-implantation rise in 3$ bet

No description available.