Physiological evidence for the existence of prolactin releasing factor: stress-induced prolactin secretion is not linked to dopaminergic receptors.

Experiments were undertaken to demonstrate the existence of a physiological role of prolactin releasing factor (PRF). Hypothalamic control of prolactin secretion is achieved by secretion of prolactin inhibiting factor (PIF) and/or PRF. Since the putative PIF is dopamine, complete blockage of the dopaminergic PIF receptors should permit demonstration of PRF activity. The changes in prolactin concentration were monitored by taking a blood sample every 2 min through an indwelling atrial cannula. An excessive amount of pimozide (3 mg/kg) was used to block dopaminergic receptors and prolactin concentration was elevated as a result. This higher concentration of circulating prolactin was maintained for more than 30 h after a bolus injection of pimozide. In this situation, lacking functional dopaminergic PIF receptors, there were fluctuations in the circulating prolactin concentration throughout the experiment. If, after pimozide administration, rats were exposed to an acute (ether) stress, the stress consistently elevated the circulating prolactin concentration. Since there are no functional dopaminergic PIF receptors available under these conditions, a dopaminergic PIF cannot be involved in producing the prolactin surge induced by the acute stress. Therefore, these results suggest that a physiological PRF is involved in the generation of this prolactin surge, through the evidence is not direct.