MECHANISM OF THE PROLACTIN REBOUND AFTER DOPAMINE WITHDRAWAL IN RAT PITUITARY-CELLS

To study the mechanism underlying the effect of dopamine withdrawal on prolactin release, continuous perifusion experiments were performed on rat lactotroph-enriched primary cultures. Removal of dopamine (10(-7) M) after a short-term application (15 min) produced a rebound of prolactin secretion, which was enhanced by pretreatment of the cell culture with 17beta-estradiol (10(-8) M for 48 h). Ca2+ channel blockade by Co2+ (1 mM) abolished the rebound in prolactin release. An increase in intracellular adenosine 3',5'-cyclic monophosphate by either forskolin (5 muM) or 3-isobutyl-1-methylxanthine (100 muM) enhanced the prolactin rebound after dopamine withdrawal. Application of thyrotropin-releasing hormone (10-7 M) increased the prolactin rebound after dopamine withdrawal with a maximum effect obtained by commencing treatment immediately after removal of dopamine. Pretreatment of cell cultures with pertussis toxin (100 ng/ml, for 10 h) totally abolished the effects of dopamine on prolactin secretion. The dopamine agonist bromocriptine (10(-9) M) significantly decreased prolactin secretion, but no rebound effect was observed after its removal. We conclude that the rebound of prolactin release after dopamine treatment involves the influx of Ca2+.