FIGURE 14 Plasma prolactin concentrations in three women during nursing and anticipation of nursing. Note that, although anticipation of nursing apparently resulted in oxytocin secretion, increased prolactin secretion did not occur until well after suckling began. (From Noel GL, Suh HK, Franz AG. J Clin Endocrinol Metab 1974; 38:413. With permission.)

Emotional signals that release oxytocin and produce milk letdown are not followed by prolactin secretion. It is unlikely that prolactin secreted during suckling can act quickly enough to increase milk production to meet current demands. Rather, such episodes of secretion are important for producing the milk needed for subsequent feedings. Milk production is thus related to frequency of suckling, which gives the newborn some control over its nutritional supply and is an extension into the postnatal period of the self-serving control over maternal function that the fetus exercised in utero.

Increased secretion of prolactin and even milk production do not require a preceding pregnancy. Repeated stimulation of the nipples can induce lactation in some women who have never borne a child. In some cultures, postmenopausal women act as wet nurses for infants whose mothers produce inadequate milk. This fact underscores the lack of involvement of the ovarian steroids in lactation once the glandular apparatus has been formed.

Prolactin is unique among the anterior pituitary hormones in the respect that its secretion is increased rather than decreased when the vascular connection between the pituitary gland and the hypothalamus is interrupted. Prolactin secretion is controlled primarily by an inhibitory hypophysiotropic hormone, dopamine. Dopamine is synthesized by sequential hydroxylation and decarbox-ylation of tyrosine (see Fig. 21 in Chapter 40). Surgical transection of the human pituitary stalk increases plasma prolactin concentrations in peripheral blood (hyper-prolactinemia) and may lead to the onset of lactation. Stimulation of prolactin secretion by suckling results from inhibition of dopamine secretion into the hypophy-sial portal circulation by dopaminergic neurons whose cell bodies are located in the arcuate nuclei. It has been found experimentally that abrupt relief from dopamine inhibition results in a surge of prolactin secretion. It is possible that prolactin secretion is also under positive control by way of a yet to be identified prolactin-releasing factor. Experimentally, prolactin secretion is increased by neuropeptides such as thyrotropin-releasing hormone (TRH) and vasoactive inhibitory peptide (VIP). In spite of its potency as a prolactin-releasing agent, it is unlikely that TRH is a physiological regulator of prolactin secretion. Normally, TSH and prolactin are secreted independently. TSH secretion does not increase during lactation. The physiological importance of VIP as a prolactin-releasing hormone has not been established.

Lactotropes express estrogen receptors and increase their production of prolactin mRNA and protein in response to estrogens. Estradiol, which stimulates proliferation and hypertrophy of lactotropes, is probably responsible for the increased number of lactotropes in the pituitary and their prolactin content during pregnancy. Estradiol may therefore increase prolactin secretion by increasing its availability. In addition, although it does not act directly as a prolactin-releasing factor, estradiol decreases the sensitivity of lactotropes to dopamine. Paradoxically, however, estradiol also increases dopamine synthesis and concentration in the hypothalamus and may therefore increase dopamine secretion (Fig. 15).

suckling stimulus sleep \

stress sleep \

TRH PRL releasing factors?

hypothalamus - .

TRH PRL releasing factors?


FIGURE 15 Control of prolactin secretion. Dashed line indicates inhibition. A physiological role for TRH (thyrotropin-releasing hormone) and other postulated releasing hormones has not been established. Estradiol stimulates secretion and may interfere with the inhibitory action of dopamine.



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