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      Caudal Hindbrain Glucoprivation Enhances γ-Aminobutyric Acid Release in Discrete Septopreoptic Structures in the Steroid-Primed Ovariectomized Rat Brain: Role of μ Opioid Receptors

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          Abstract

          The neurochemical mechanisms underlying hindbrain glucoprivic suppression of the luteinizing hormone (LH) surge are not known. A body of experimental evidence supports the view that gonadal steroid positive-feedback action on the reproductive neuroendocrine axis relieves tonic GABAergic inhibition of gonadotropin-releasing hormone neurons by diminishing preoptic release of this neurotransmitter. The present studies evaluated the hypothesis that hindbrain glucoprivic attenuation of the LH surge may be correlated with site-specific modifications in gonadal steroid suppression of γ-aminobutyric acid release in this region of the brain. Individual septopreoptic loci were microdissected from the brains of estrogen, progesterone-primed ovariectomized female rats injected with the glucose antimetabolite, 5-thioglucose (5-TG), or vehicle into the caudal fourth ventricle during the ascending phase of the surge, and analyzed by high-performance liquid chromatography. The data show that 5- TG administration increased GABA release within the rostral preoptic area (rPO), anteroventral periventricular nucleus (AVPV), and median preoptic nucleus (MEPO), relative to the vehicle-treated controls, but did not alter neurotransmitter release in other structures evaluated. The rate of GABA turnover in each brain site was equivalent between animals injected with the µ opioid receptor antagonist CTOP and 5-TG versus their vehicle-treated controls. These results constitute novel evidence for site-specific modulation of steroid positive-feedback suppression of this inhibitory neurotransmitter by caudal hindbrain signaling of glucose insufficiency, and support the need for neurochemical characterization of glucoprivic-sensitive afferent input to GABAergic neurons terminating within the rPO, AVPV, and MEPO, as well as the relevance of enhanced local GABA release for reproductive neuroendocrine function.

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          Most cited references 23

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          Metabolic fuels and reproduction in female mammals

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            Discrete Lesions Reveal Functional Heterogeneity of Suprachiasmatic Structures in Regulation of Gonadotropin Secretion in the Female Rat

            The present study examines the function of several cytologically distinct suprachiasmatic structures in the regulation of ovulation and positive feedback effects of estrogen and progesterone on gonadotropin release in the rat. Small (0.6–0.8 mm dia.) electrolytic lesions were placed at four loci along the rostrocaudal extent of the suprachiasmatic region in regularly cycling female rats. Anovulatory persistent estrus occurred only when lesions were located either in the suprachiasmatic nucleus (SCN) or the medial preoptic nucleus (MPN), a small periventricular cell group lying immediately caudal to the organum vasculosum lamina terminalis (OVLT). Lesions restricted to the OVLT and adjacent ventral prechiasmatic region (VPC-L), or the anterior suprachiasmatic region (ASR) between the MPN and SCN resulted in irregular estrous cycles frequently marked by periods of prolonged diestrus. Following administration of 50 µg estradiol benzoate (EB) a daily afternoon surge of gonadotropin was observed in control animals. This circadian release of gonadotropins was completely abolished by SCN, ASR and MPN lesions. EB-induced gonadotropin surges were also greatly attenuated by VPC-L lesions. Subsequent administration of 1.5 mg progesterone (P) induced large surges of luteinizing hormone and follicle-stimulating hormone in VPC-L and ASR lesioned animals as well as controls. P administration also elicited gonadotropin surges in SCN lesioned animals, although surges were markedly attenuated in magnitude compared to controls. Only lesions that destroyed the MPN and immediately adjacent periventricular tissue completely and invariably eliminated P-induced gonadotropin release. Thus, anovulatory persistent estrus appears to be associated specifically with lesions that interfere with the positive feedback effect of P (MPN and SCN lesions). Animals with lesions that block or attenuate EB effects without interfering with P sensitive neural substrates can maintain long-term spontaneous ovulation (VPC-L and ASR lesions). An hypothesis is advanced to account for the differential effect of MPN and SCN lesions on P-induced gonadotropin release.
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              Immunohistochemical localization of mu-opioid receptors in the central nervous system of the rat.

              Of the three major types of opioid receptors ( mu, delta, kappa) in the nervous system, mu-opioid receptor shows the highest affinity for morphine that exerts powerful effects on nociceptive, autonomic, and psychological functions. So far, at least two isoforms of mu-opioid receptors have been cloned from rat brain. The present study attempted to examine immunohistochemically the distribution of mu-opioid receptors in the rat central nervous system with two kinds of antibodies to recently cloned mu-opioid receptors (MOR1 and MOR1B). One antibody recognized a specific site for MOR1, and the other bound to a common site for MOR1 and MOR1B. Intense MOR1-like immunoreactivity (LI) was seen in the 'patch' areas and subcallosal streak in the striatum, medial habenular nucleus, medial terminal nucleus of the accessory optic tract, interpeduncular nucleus, median raphe nucleus, parabrachial nuclei, locus coeruleus, ambiguous nucleus, nucleus of the solitary tract, and laminae I and II of the medullary and spinal dorsal horns. Many other regions, including the cerebral cortex, amygdala, thalamus, and hypothalamus, also contained many neuronal elements with MOR1-LI. The distribution pattern of the immunoreactivity revealed with the antibody to the common site for MOR1 and MOR1B (MOR1/1B-LI) was almost the same as that of MOR1-LI. Both MOR1-LI and MOR1/1B-LI were primarily located in neuronal cell bodies and dendrites. However, the immunoreactivities were observed in the accessory optic tract, fasciculus retroflexus, solitary tract, and primary afferent fibers in the superficial layers of the medullary and spinal dorsal horns. The presynaptic location of MOR1-LI and MOR1/1B-LI was confirmed by lesion experiments: Enucleation, placing a lesion in the medial habenular nucleus, removal of the nodose ganglion, or dorsal rhizotomy resulted in a clear reduction of the immunoreactivities, respectively, in the nuclei of the accessory optic tract, some subnuclei of the interpeduncular nucleus, nucleus of the solitary tract, or laminae I and II of the spinal dorsal horn. The results indicate that the mu-opioid receptors are widely distributed in the brain and spinal cord, mainly postsynaptically and occasionally presynaptically. Opioids, including morphine, may inhibit the excitation of neurons via the postsynaptic mu-opioid receptors, and also suppress the release of neurotransmitters and/or neuromodulators from axon terminals through the presynaptic mu-opioid receptors.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2004
                January 2005
                25 January 2005
                : 80
                : 4
                : 201-209
                Affiliations
                Department of Basic Pharmaceutical Sciences, School of Pharmacy, College of Health Sciences, University of Louisiana, Monroe, La., USA
                Article
                82544 Neuroendocrinology 2004;80:201–209
                10.1159/000082544
                15591795
                © 2004 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: 5, Tables: 3, References: 35, Pages: 9
                Categories
                Original Paper

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