Stimulation of prolactin release by dopamine withdrawal: role of calcium influx

Stimulation of prolactin release by dopamine withdrawal: role of calcium influx. Am. J. PhysioZ. 267 (EndocrinoZ. Metab. 30): E789-E794, 1994.Withdrawal of dopamine (DA), a neuro-transmitter that inhibits prolactin (PRL) release from the anterior pituitary, stimulates PRL release with transient (30-to 45min) secretory rates that exceed those observed before application of DA (“PRL rebound”). Using patch-clamp meth-ods on identified rat lactotropes, we have demonstrated that a period of increased Ca2+-spiking activity follows recovery from the DA-induced hyperpolarization. The present experiments used dissociated pituitary cells to identify the relative roles of adenosine 3’,5’-cyclic monophosphate (CAMP), inositol phos-phates, and the enhanced influx of Ca2+ in the rebound secretion of PRL. Rebound secretion of PRL after DA with-drawal was completely blocked by the Ca2+ channel blocke