Abstract
Prolactin is a polypeptide hormone secreted from the lactotrophs in the anterior pituitary gland. It is recognized as a pleiotropic hormone with multiple biological actions, which seem to have evolved to provide physiological adaptations required for the success of reproduction. Among its numerous roles, lactation is one to which prolactin is essential, being the primary hormone responsible for the synthesis of milk. The neuroendocrine control of prolactin secretion is unique among the anterior pituitary hormones. The lactotrophs have a high spontaneous capacity for proliferation and secretion of prolactin that is suppressed by dopamine. Neuroendocrine dopaminergic (NEDA) neurons release dopamine into the hypothalamic-pituitary portal blood system to inhibit prolactin secretion. Prolactin exerts a short-loop negative feedback effect stimulating several aspects of NEDA neuronal activity, resulting in inhibition of its own secretion. The nipple suckling by the offspring during lactation is the most powerful stimulus to increase prolactin secretion. Thus, lactation is a hyperprolactinemic state, characterized by suckling-induced prolactin surges and chronically elevated basal levels of prolactin. Phenotypic and functional modifications in the NEDA neurons associated with changes in the number and organization of lactotrophs are responsible for the remarkable increase in prolactin secretion during lactation. Hypothalamic prolactin-releasing factors seem to also stimulate the rise in prolactin secretion, but their identity remains to be determined. In this chapter, we review the classical concepts and recent advances in our understanding of the neuroendocrine control of prolactin secretion and how it changes to promote the physiological state of hyperprolactinemia during lactation.