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Rapid Augmentation of Prolactin Cell Number and Secretory Capacity by an Estrogen-Induced Factor Released from the Neurointermediate Lobe^*

Division of Molecular and Cellular Endocrinology, Department of Anatomy and Cell Biology, Medical University of South Carolina Charleston, South Carolina 29425

Address all correspondence and requests for reprints to: Dr. L. Stephen Frawley, Department of Anatomy and Cell Biology, Medical University of South Carolina, 171 Ashley Avenue, Charleston, South Carolina 29425.

Abstract

17β-Estradiol (E₂) has been shown to exert an acute stimulatory effect on PRL secretion via an indirect action involving the neurointermediate lobe (NIL). In the present study we used a reverse hemolytic plaque assay to determine whether this effect was manifested as an augmentation of the number of PRL secretors and/or an increase in the amount of hormone released per PRL cell. Cultures of anterior pituitary (AP) and NIL cells from ovariectomized rats were cultured overnight, exposed to the treatment (E₂ or vehicle) for 3 h, and then subjected to a reverse hemolytic plaque assay that was carried out in the presence or absence of TRH. Concurrent exposure of AP cells to E₂ and NIL cells evoked an 11–12% increase in the overall proportion of PRL-secreting cells. This was true when the AP and NIL cells were incubated as a mixed culture and when the two cell types were maintained in the same petri dish but on separate plastic supports, and TRH did not significantly influence this response. The effect of E₂ on the number of PRL secretors was negated when NIL cells were not present throughout the experiment or when they were removed from the cultures just before commencement of E₂ treatment. Simultaneous treatment with E₂ and NIL cells also significantly augmented the sizes of PRL plaques produced under basal conditions by AP cells. Taken together, these results demonstrate that E₂ stimulates NIL cells to release an activity that enhances PRL secretion in two ways: 1) by recruiting additional PRL cells into the secretory pool, and 2) by augmenting the secretory capacity of individual PRL cells.

Footnotes

^* This work was supported by NIH Grant DK-38215 (to L.S.F.)

Received March 8, 1991.

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