The roles of dopamine and the neurointermediate lobe of the pituitary in the regulation of prolactin secretion during late pregnancy in rats

The major hypothalamic control over prolactin secretion from the anterior pituitary gland is inhibitory by means of dopamine released from tuberoinfundibular dopamine (TIDA) neurones. We have previously shown a dissociation between activity of TIDA neurones and prolactin secretion during late pregnancy, suggesting involvement of additional regulatory factors. The aim of the present study was to investigate the role of dopamine and the neurointermediate lobe (NIL) of the pituitary in the regulation of prolactin secretion during late pregnancy. To determine whether dopamine maintains inhibition of prolactin during late pregnancy, the D-2 receptor antagonist domperidone was administered at 12.00 h on days 18 and 21 of pregnancy. These times are characterized by high and low TIDA neuronal activity, respectively, and low prolactin secretion. Domperidone produced an immediate increase in plasma prolactin compared to vehicle-treated controls on both days 18 and 21. Thus, dopaminergic inhibition of prolactin secretion is maintained despite reduced TIDA neuronal activity at the end of pregnancy. The contribution of NIL-derived dopamine in regulating prolactin secretion was then examined by investigating the effect of surgical removal of the NIL. NIL removal produced significantly increased basal prolactin concentrations, indicating that dopamine from the NIL contributes to the suppression of prolactin before the antepartum prolactin surge. Furthermore, NIL removal also completely prevented the antepartum prolactin surge compared to sham-operated controls, which is consistent with the hypothesis that the NIL supplies a prolactin-releasing factor to the anterior pituitary to induce the antepartum prolactin surge.