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      An Opioid Pathway in the Hypothalamus of the Turkey That Stimulates Prolactin Secretion

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          Abstract

          Circulating prolactin (PRL) levels increase when dynorphin is infused into the turkey brain. This study tested the hypothesis that centrally infused dynorphin requires an intact vasoactive intestinal peptide (VIP) system in order to stimulate turkey PRL secretion. It also investigated the roles of the dopaminergic and serotonergic systems in dynorphin-induced PRL release. Drugs were infused into the third ventricle of anesthetized laying turkeys via stereotaxically guided cannulae and circulating blood was assayed for changes in PRL levels. When a highly selective ĸ opioid receptor antagonist was given prior to dynorphin injection, the PRL response to dynorphin was almost totally blocked. The coinfusion of either a serotonin (5-HT) or a D<sub>1</sub> dopamine (DA) receptor antagonist with dynorphin prevented the increase in PRL observed in birds when dynorphin was infused alone. On the other hand, the ĸ opioid receptor antagonist failed to prevent the 5-HT-induced release of PRL. In hens actively immunized against VIP, infused dynorphin was unable to increase plasma PRL levels and infused VIP gave a muted PRL rise, while large increases in PRL were seen in nonimmunized birds receiving the same infusions. These data show that: (1) dynorphin stimulates PRL secretion by activating ĸ opioid receptors in the avian hypothalamus, and (2) dynorphin, 5-HT, DA, and VIP stimulate avian PRL secretion via a common pathway expressing ĸ opioid, serotonergic, dopaminergic, and VIPergic receptors at synapses arranged serially in that functional order, with the VIPergic system as the final mediator (releasing factor).

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          Most cited references 13

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          The stimulatory and inhibitory effects of dopamine on prolactin secretion in the turkey.

          Dopamine (DA) was infused into the third ventricle of anesthetized laying turkey hens at various concentrations to determine its effect on both basal prolactin (PRL) levels and ongoing electrically induced PRL secretion. The infusion of DA at rates of 1.0 or 10.0 nmol/min resulted in dose dependent increases in plasma PRL. These infusions had no inhibitory effect on electrically stimulated PRL release. The infusion of DA at 100.0 or 500.0 nmol/min caused no stimulation of PRL secretion and totally inhibited the PRL response elicited by electrical stimulation of the medial preoptic nucleus. These results show that dopaminergic influences are involved in both stimulating and inhibiting avian PRL secretion and suggest possible biphasic actions of DA within the brain.
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            Regulation of Prolactin Secretion by Dopamine and Vasoactive Intestinal Peptide at the Level of the Pituitary in the Turkey

            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 ± 15.1 to 181.3 ± 44.3 ng/ml, p 2 DA receptor agonist R- (–) -Propylnorapomorphine HCl inhibited VIP-induced PRL secretion at the level of the anterior pituitary, allowing only an insignificant rise in PRL (54.8 ± 14.3 to 73.9 ± 21.6 ng/ml, p > 0.05), while the D 1 DA receptor agonist (±)-SKF-38393 HCl failed to prevent VIP-induced PRL release, allowing PRL to rise 2.5-fold (49.1 ± 10.8 to 121.0 ± 34.8 ng/ml, p 2 DA receptors residing within the anterior pituitary. The data also suggested that there were no stimulatory D 1 DA receptors related to PRL secretion in the avian anterior pituitary.
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              Morphine- and opioid peptide-induced inhibition of the release of dopamine from tuberoinfundibular neurons

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                1999
                November 1999
                17 November 1999
                : 70
                : 5
                : 317-323
                Affiliations
                aDepartment of Animal Science, University of Minnesota, St.Paul, Minn., USA; bDepartment of Medicine, University of Virginia, Charlottesville, Va., USA
                Article
                54492 Neuroendocrinology 1999;70:317–323
                10.1159/000054492
                10567857
                © 1999 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, References: 47, Pages: 7
                Categories
                Functional Neuroanatomy of Hypothalamic Neurons

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