AJP - Endocrinology and Metabolism, Vol 265, Issue 1 E145-E152, Copyright © 1993 by American Physiological Society
Mechanism of the prolactin rebound after dopamine withdrawal in rat pituitary cells
C. Chen, J. Zhang, J. M. Israel, I. J. Clarke and J. D. Vincent
Prince Henry's Institute of Medical Research, Clayton, Victoria, Australia.
To study the mechanism underlying the effect of dopamine withdrawal on
prolactin release, continuous perfusion 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 17
beta-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 microM) or
3-isobutyl-1-methylxanthine (100 microM) 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+.
