Introduction

The use of pharmacological agents in neuroendocrine studies had a significant impact on our perception of the control mechanisms involved in prolactin secretion. In contrast to other anterior pituitary hormones, prolactin is thought to be regulated by the hypothalamus through a prolactin inhibiting factor (PIF) a peptide of MW < 5000 that is tonically released into the hypophysial portal vessels. The prolactin secretory cells themselves are assumed to be driven by a prolactin releasing factor (PRF), an unidentified as yet neurosecretory product. PRF neurosecretory cells are in turn thought to be driven by serotoninergic neurons located in the medial basal hypothalamus.

Of the major CNS neurotransmitters dopamine is a potent inhibitor of prolactin release, although the exact nature of the interaction between the PIF and dopamine is at best unclear at present. The original postulate that PIF secretion is stimulated by dopaminergic neurons located in the medial basal hypothalamus is challenged by the fact that dopamine receptors have been located on the prolactin secretory cells (Clemens, 1976). The emerging synthetic view of the problem postulates that the PIF secreting cells act in parallel and are at the same time driven by the dopaminergic neurons of the medial basal hypothalamus (Fig. 33.1).

Serotonin is the other major CNS neurotransmitter involved in the control of prolactin secretion. It is again as yet unclear whether serotonin stimulates prolactin secretion by inhibiting the PIF release or by stimulating PRF release.