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Endocrinology, Vol 130, 133-138, Copyright © 1992 by Endocrine Society
ARTICLES |
E Ellerkmann, GM Nagy and LS Frawley
Department of Anatomy and Cell Biology, Medical University of South Carolina, Charleston 29425.
When neurointermediate lobe (NIL) cells from ovariectomized rats are exposed to 17 beta-estradiol (E2) in vitro, they release a substance that rapidly induces the recruitment of additional PRL cells into the secretory pool. In the present study we tested the hypothesis that this mammotrophic factor is alpha MSH. Cocultures of anterior pituitary and NIL cells were incubated for 18 h, exposed to various treatments for 3 h, and then subjected to a reverse hemolytic plaque assay to quantify the percentage of all pituitary cells that released PRL. Combined exposure to E2 and NIL cells caused a significant increase in the fraction of anterior pituitary cells that released PRL, and the presence of TRH during the reverse hemolytic plaque assay did not affect the magnitude of the response. Treatment with dopamine (which inhibits alpha MSH release) reversed the recruitment of PRL secretors induced by E2 stimulation of NIL cells. Likewise, immunoneutralization with an antiserum directed against alpha MSH abolished the response. Furthermore, alpha MSH alone could substitute for E2 and NIL cells in evoking the recruitment response, whereas none of several other POMC- derived peptides had any consistent effect. Taken together, these results demonstrate that alpha MSH is a mammotrophic factor released by NIL cells in response to E2.
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