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 17β-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 μM) or 3-isobutyl-1- methylxanthine (100 μM) 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+.
|Number of pages||8|
|Journal||American Journal of Physiology|
|Issue number||1 28-1|
|Publication status||Published - 1 Jan 1993|
- adenosine 3',5'-cyclic monophosphate
- G protein
- thyrotropin-releasing hormone