The preovulatory prolactin surge: an evaluation of the role of dopamine

This study examined the contribution of dopamine (DA) to the control of PRL secretion during the preovulatory PRL surge. Immature female rats were injected with PMSG on day 28. At selected times during the periovulatory period, rats were injected with different pharmacological agents, and jugular blood was collected at frequent intervals. Blood PRL levels in vehicle-treated rats were low on the morning of day 30, rose 15- to 20-fold to peak levels from 1400-1500 h, were maintained at a plateau from 1900-2300 h, and were reduced to basal levels on the morning of day 31. Haloperidol, a DA antagonist, induced a 20-fold rise in PRL before the surge, a 2-fold rise above peak PRL levels at 1500 h, and a 50-fold rise on the morning of day 31. In contrast, haloperidol failed to alter PRL release during the plateau phase. Apomorphine, a DA agonist, reduced PRL levels when injected during either the peak or the plateau phase. Injection of 5-hydroxytryptophan, a serotonin precursor, increased PRL levels at all times examined. Anterior pituitary PRL content was reduced to 30% and 10% of the presurge level during the peak and plateau phases, respectively, but increased on the morning of day 31. Basal PRL release by hemipituitaries incubated in vitro paralleled the anterior pituitary PRL content, with markedly less PRL secreted during the peak and plateau phases compared to the presurge period. However, the percent inhibition of PRL release by hemipituitaries incubated with 50 nM DA was similar at all times tested. These data indicate that the peak PRL surge occurs in spite of DA input to the anterior pituitary, a continued responsiveness to DA inhibition, and a diminishing pituitary PRL content. We conclude that a nondopaminergic mechanism, possibly involving a PRL-releasing factor, is responsible for the peak. The plateau phase probably results from an absence of DA input to the anterior pituitary together with a reduction in the releasable pool of PRL. The termination of the PRL surge is caused by the restoration of DA input.