scholarly journals Thyrotropin-releasing Hormone Stimulation of Prolactin Release from Clonal Rat Pituitary Cells

1981 ◽  
Vol 67 (6) ◽  
pp. 1769-1776 ◽  
Author(s):  
Marvin C. Gershengorn ◽  
Sylvia T. Hoffstein ◽  
Mario J. Rebecchi ◽  
Elizabeth Geras ◽  
Brian G. Rubin
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Hormone Stimulation ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Stimulation Of

Extracellular ATP as an autocrine/paracrine regulator of prolactin release

1997 ◽  
Vol 272 (6) ◽  
pp. E1117-E1123 ◽  
Author(s):  
L. Nunez ◽  
C. Villalobos ◽  
L. S. Frawley
Keyword(s):  
Secretory Granules ◽  
Extracellular Atp ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Cells Cultured ◽  
Local Regulator

Recent evidence demonstrates that ATP, costored with a number of hormones and neurotransmitters in secretory granules, is coreleased during exocytosis of these agents. Here, we explored the possibility that extracellular ATP subserves an autocrine and/or paracrine role in the regulation of prolactin (PRL) release by subjecting rat pituitary cells to various experimental manipulations aimed at evaluating putative interactions between ATP and mammotropes. Our results strongly support the view that ATP functions as a local regulator of PRL secretion. To be more specific, we observed that ATP is released in a predictable manner by physiologically relevant secretagogues that are reasonably targeted to mammotropes. Moreover, we found that ATP can act directly on pituitary cells to stimulate the release of PRL from most (if not all) mammotropes. Finally, we determined that antagonism or removal of ATP leads to a diminution of PRL export from pituitary cells cultured under basal or thyrotropin-releasing hormone-stimulated conditions. On the basis of these results, we propose that ATP acts locally to amplify and prolong the PRL secretory response elicited by a more traditional hypophysiotropic signal.

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