Role of dopamine and vasoactive intestinal peptide in the control of pulsatile prolactin secretion.

The present studies were designed to obtain a detailed characterization of pulsatile PRL secretory patterns under basal conditions and to explore the role of dopamine (DA) and vasoactive intestinal peptide (VIP) in the genesis of PRL pulses. Adult intact male rats received chronic indwelling jugular canula and were bled at 3-min intervals for periods ranging from 90-150 min. Pulse analysis was performed using the algorithm Detect. Blockade of DA receptors with domperidone, pimozide, or haloperidol resulted in a 2-fold increase in PRL pulse frequency, with no change in pulse duration. All quantitative parameters, i.e. peak and trough values, pulse amplitude, and area under the pulse, were significantly increased after dopaminergic blockade. Blockade of endogenous VIP activity was achieved by passive immunization with a potent VIP antiserum. This treatment, by itself, did not modify basal PRL levels or PRL pulsatility parameters. However, when VIP antiserum was administered in combination with domperidone, a reduction in all quantitative pulse parameters was observed. Heterogeneity of PRL pulses was evaluated by frequency distribution analysis, using the area under the pulse divided by basal secretion, to evaluate the mass of hormone secreted per pulse normalized to the basal rate of secretion. Untreated animals presented pulses within a range of different masses. Dopaminergic blockade resulted in a great reduction in big mass pulses, and the distribution of pulses was restricted primarily to small mass pulses. The increased pulse frequency after dopaminergic blockade, therefore, results mainly from an increase in the appearance of small mass pulses. These results indicate that DA exerts a tonic inhibitory action on the frequency as well as the qualitative parameters of PRL pulses. They also suggest that big mass PRL pulses are dopaminergic in origin, i.e. they may result from temporary interruptions in DA activity. Small mass PRL pulses appear to result from other neural stimulatory inputs. Endogenous VIP enhances quantitative PRL pulse parameters, but this activity is only apparent after removal of DA inhibition.