title: Somatostatin does not inhibit prolactin synthesis in normal male rat pituitary cells but inhibits prolactin synthesis in estradiol-primed pituitary cells.
abstract: The effects of somatostatin (SRIF) on prolactin (PRL) synthesis and release were examined in primary cultured pituitary cells derived from normal and estradiol (E2)-primed male rat pituitaries. The cells were continuously incubated in a pulse medium containing [3H]leucine with or without 10(-6) mol/l SRIF for a period of 15, 30, 60, 180 or 360 min. Following incubation, the medium was recovered and the cells were fractionated into cytosolic and granular fractions. PRL was isolated by SDS-PAGE and newly synthesized PRL ([3H]PRL) was identified by coincident peaks of tritium activities and PRL contents. The specific activity (SA, c.p.m./ng), a ratio of [3H]PRL to total PRL, was determined for the granular, cytosolic and medium fractions. In control and SRIF-treated groups of non-primed pituitary cells, SAs of all three fractions significantly increased during the 6-h incubation. Cytosolic and granular SAs showed similar profiles of increasing rate in comparison to control. Medium SAs showed a significantly higher value in the SRIF-treated group than in the control group only at 180 min. These observations indicate that, in the non-primed condition, PRL synthesis is not inhibited by SRIF. Medium SAs in the E2-primed group were significantly higher than SAs in the non-primed control cells during the initial 3 h of incubation, and cytosolic and granular SAs were significantly higher than those of the non-primed control during the 3- to 6-h incubation period. These observations demonstrate that E2 enhances PRL synthesis and secretion of newly synthesized PRL. SRIF treatment of E2-primed lactotrophs resulted in a significant decrease in SAs of all three fractions as compared with those of the E2-primed control. Our results indicate that in normal male rat pituitary cells SRIF does not inhibit PRL synthesis but effectively inhibits PRL synthesis in E2-primed lactotrophs. This suggests that the inhibitory action of SRIF on PRL synthesis is estrogen dependent.
authors.affiliation: Department of Physiology, Queen's University, Kingston, Ontario, Canada.
authors.forename: S C
authors.initials: SC
authors.lastname: Lee
authors.forename: S H
authors.initials: SH
authors.lastname: Shin
mesh_terms: D000818:Animals; D018929:Cell Culture Techniques; D003864:Depression, Chemical; D004591:Electrophoresis, Polyacrylamide Gel; D004958:Estradiol / Q000494:pharmacology*; D008297:Male; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D011388:Prolactin / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013004:Somatostatin / Q000494:pharmacology*
chemical_list: D004958:Estradiol; D013004:Somatostatin; D011388:Prolactin