{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,7]],"date-time":"2026-06-07T18:17:09Z","timestamp":1780856229412,"version":"3.54.1"},"reference-count":11,"publisher":"S. Karger AG","issue":"5","license":[{"start":{"date-parts":[[1998,1,1]],"date-time":"1998-01-01T00:00:00Z","timestamp":883612800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[1998,1,1]],"date-time":"1998-01-01T00:00:00Z","timestamp":883612800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuroendocrinology"],"published-print":{"date-parts":[[1998]]},"abstract":"This study investigated the capability of dopamine (DA) to prevent avian prolactin (PRL) secretion by antagonizing the PRL-releasing factor, vasoactive intestinal peptide (VIP), at the level of the pituitary. To test this hypothesis, combined intracranial and intrapituitary infusions of DA, DA agonists, and VIP, plus electrical stimulation of the medial preoptic area (ES\/POM), were used to characterize the actions of DA on PRL secretion in anesthetized laying turkey hens. Infused into the third ventricle at the rate of 10 nmol\/min, DA induced a 2.8-fold increase in circulating PRL levels (63.8 \u00b1 15.1 to 181.3 \u00b1 44.3 ng\/ml, p < 0.05), similar to the 3.1-fold PRL increase induced by ES\/POM (65 \u00b1 10.3 to 199.1 \u00b1 57.3 ng\/ml, p < 0.05). Infused into the anterior pituitary at the rate of 15 ng\/min, VIP induced a 2.2-fold increase in PRL (78.6 \u00b1 22.9 to 173.6 \u00b1 39.5 ng\/ml, p < 0.05). When DA (10 nmol\/min) was infused into the anterior pituitary it completely blocked both ES\/POM- and VIP-induced PRL secretion. The D<sub>2<\/sub> DA receptor agonist R- (\u2013) -Propylnorapomorphine HCl inhibited VIP-induced PRL secretion at the level of the anterior pituitary, allowing only an insignificant rise in PRL (54.8 \u00b1 14.3 to 73.9 \u00b1 21.6 ng\/ml, p > 0.05), while the D<sub>1<\/sub> DA receptor agonist (\u00b1)-SKF-38393 HCl failed to prevent VIP-induced PRL release, allowing PRL to rise 2.5-fold (49.1 \u00b1 10.8 to 121.0 \u00b1 34.8 ng\/ml, p < 0.05). Pituitary infusion of DA, DA agonists or vehicle alone caused no change in PRL levels. The data showed that DA prevented avian PRL secretion by blocking the action of VIP at the level of the anterior pituitary. DA effected this blockade of PRL via D<sub>2<\/sub> DA receptors residing within the anterior pituitary. The data also suggested that there were no stimulatory D<sub>1<\/sub> DA receptors related to PRL secretion in the avian anterior pituitary.<\/jats:p>","DOI":"10.1159\/000054380","type":"journal-article","created":{"date-parts":[[2003,4,15]],"date-time":"2003-04-15T19:06:20Z","timestamp":1050433580000},"page":"319-325","source":"Crossref","is-referenced-by-count":44,"title":["Regulation of Prolactin Secretion by Dopamine and Vasoactive Intestinal Peptide at the Level of the Pituitary in the Turkey"],"prefix":"10.1159","volume":"68","author":[{"given":"Orlan M.","family":"Youngren","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yupaporn","family":"Chaiseha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed E.","family":"El Halawani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[1998,11,18]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1006\/gcen.1995.1049"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1006\/gcen.1994.1130"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(87)90352-9"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(87)90082-3"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(87)90604-2"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1038\/347072a0"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1038\/350614a0"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.13.7156"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1016\/0301-0082(89)90008-7"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1006\/gcen.1993.1121"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.8.4005"}],"container-title":["Neuroendocrinology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/54380","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/54380","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:26:22Z","timestamp":1745468782000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000054380"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1998]]},"references-count":11,"journal-issue":{"issue":"5","published-online":{"date-parts":[[1998,11,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000054380","archive":["Portico"],"relation":{},"ISSN":["0028-3835","1423-0194"],"issn-type":[{"value":"0028-3835","type":"print"},{"value":"1423-0194","type":"electronic"}],"subject":[],"published":{"date-parts":[[1998]]}}}