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      Immunoneutralization of Endogenous Opioid Peptides Prevents the Suckling-Induced Prolactin Increase and the Inhibition of Tuberoinfundibular Dopaminergic Neurons

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          Abstract

          Previous studies have shown that the endogenous opioid peptides, acting at specific opiate receptor subtypes, are involved in the suckling-induced prolactin secretory response. The prolactin increase elicited by suckling is due, at least in part, to an inhibition of tuberoinfundibular dopaminergic (TIDA) neurons in the hypothalamus. We investigated the effects of immunoneutralization of dynorphin, leu-enkephalin and met-enkephalin on the suckling-induced prolactin increase and on the activity of the TIDA neurons in lactating female rats between days 7 and 12 postpartum. Rats were injected into the right lateral ventricle with antiserum specific for one of these three peptides. Control rats were administered equal amounts of immunoglobulin proteins. Suckling produced a profound and significant increase in prolactin levels, as well as a decrease in DOPA accumulation in the median eminence of lactating rats. Administration of immunoglobulin concentrations of up to 3.6 µg did not inhibit the prolactin secretory response to the suckling stimulus and did not prevent the suckling-induced inhibition of TIDA neurons. Antisera to all three endogenous opioid peptides abolished the suckling-induced prolactin increase and prevented the inhibition in DOPA accumulation in the median eminence. Thus, the endogenous opioid peptides, dynorphin, leu-enkephalin and met-enkephalin, are essential for the prolactin secretory response to suckling and inhibition of TIDA neuronal activity is at least one of the mechanisms of action utilized by these peptides.

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          Most cited references 14

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          Primary structures and expression from cDNAs of rat opioid receptor δ-and μ-subtypes

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            Distinct distributions of mu, delta and kappa opioid receptor mRNA in rat brain.

            We present a comprehensive comparison of the anatomical distributions of the cloned mu, delta and kappa opioid receptor mRNA in rat brain. Northern blot analysis revealed that mRNA species encoding the three receptors differed in size and were differentially localized in brain regions. In peripheral tissues analyzed, the 3 mRNA species were detected only in the spinal cord. The distributions of mu, delta and kappa receptor mRNA in rat brain were examined by in situ hybridization histochemistry using gene-specific probes. Mu receptor mRNA was predominately localized to thalamic, brainstem and reticular core nuclei and was highest in the habenular and thalamic nuclei. In contrast, kappa receptor mRNA was expressed in hippocampus including dentate gyrus, hypothalamic and some thalamic nuclei and also present in cortex, caudate putamen, olfactory tubercle and nucleus accumbens. Delta receptor mRNA was prominent in cerebral cortex, olfactory tubercle, hippocampus, caudate putamen and nucleus accumbens. These results show that the mRNA distribution for each opioid receptor subtype in brain is unique and correlate well with the known distribution of the corresponding opioid receptor binding sites.
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              Neuroanatomical localization ofκ1and κ2 opioid receptors in rat and guinea pig brain

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2000
                April 2000
                17 April 2000
                : 71
                : 4
                : 268-276
                Affiliations
                Department of Zoology, Center for Neuroscience, Miami University, Oxford, Ohio, USA
                Article
                54545 Neuroendocrinology 2000;71:268–276
                10.1159/000054545
                10773747
                © 2000 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: 60, Pages: 9
                Categories
                Reproductive Neuroendocrinology

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