Neuroendocrinology of Lactation

Although other hormones influence the quantity of milk secretion, prolactin and adrenal corticosteroids are essential for initiating and maintaining lactation. During pregnancy high levels of estrogen and progesterone inhibit lactation, and elevation of prolactin and ACTH-adrenal corticosteroid levels result in the initiation of lactation at the end of pregnancy. Suckling maintains lactation through release of prolactin, ACTH-adrenal glucocorticoid, and oxytocin. The hypothalamus contains a prolactin-inhibiting factor (PIF) and probably also a prolactin-releasing factor (PRF). The thyrotropin-releasing factor (TRF) induces release of prolactin. Catecholamines and acetylcholine depress prolactin, and serotonin results in increased release. Estradiol, thyroxin, and thyrotropin directly cause prolactin release in vitro, while dopamine, norepinephrine, and epinephrine inhibit release although small doses may stimulate prolactin release. Ergot drugs and sodium pentobarbital inhibit in vitro prolactin release, and estradiol and ergot drugs act on the hypothalamus as well. In spontaneous galactorrheas associated with amenorrhea, high blood prolactin levels are found, while in idiopathic galactorrheas with no menstrual abnormalities the prolactin blood levels are normal. Reserpine, phenothiazine derivatives, haloperidol, and other drugs increase prolactin release, while L-dopa and ergots can inhibit lactation after parturition as well as spontaneous galactorrheas