Effects of Estrogen on Prolactin (PRL) Incorporation by Lutein and Milk Secretory Cells and on Pituitary PRL Secretion in the Postpartum Rat: Correlations with Target Cell Responsiveness to PRL1

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Abstract
The relationships between cell function and the incorporation of endogenous prolactin (PRL) by milk secretory cells (MSC) and lutein cells (LC) were examined in lactating rats which had been given graded estradiol treatment designed to dissociate progressively the activities of these two PRL target cell populations, decreasing MSC function while maintaining or augmenting LC function. MSC function was assessed by monitoring pup growth and by histological study of mammary tissue. LC function was assessed by radioimmunoassay (RIA) of circulating progesterone (P) and 20α-hydroxyprogesterone (20α) and by histological evaluation of ovaries. PRL availability was assessed by RIA of serum PRL and by morphological evaluation of pituitary PRL cells. Intracellular distributions of endogenous PRL in both target tissues were examined immunohistochemically. The availability of PRL binding sites was also examined in MSC from rats given the highest dose of estrogen. As estrogen dosage increased, PRL secretion was maintained, or increased. Despite this, there Was progressive lactational failure, accompanied by a graded failure of PRL incorporation into MSC. These cells appeared to lose, successively, their abilities to translocate PRL to nuclei, to transport it from basal to apical regions of the cell and ultimately, with the highest dose of estrogen, to internalize or even recognize PRL, as evidenced by the absence of not only PRL, but even PRL-binding sites. In contrast, as estrogen dosage increased, titers of P and P/20α ratios remained high and LC showed progressive morphological signs of not only increased activity (hypertrophy, nucleolar enlargement) but augmented incorporation of PRL. Thus, in both MSC and LC, estrogen produced a spectrum of variations in responsiveness to PRL; this spectrum was correlated with a series of effects on PRL incorporation by these cells. These estrogenic modulations of PRL action might, therefore, involve regulating the access of this protein hormone to various intracellular control points.