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      Involvement of Endogeneous Glutamate in the Stimulatory Effect of Norepinephrine and Serotonin on the Hypothalamo-Pituitary-Adrenocortical Axis

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          Abstract

          The effects of ionotropic glutamate receptor antagonists on the pituitary adrenal responses following injections of norepinephrine (NE) and serotonin (5-HT) receptor agonists into the hypothalamic paraventricular nucleus (PVN) or electrical stimulation of central NE and 5-HT pathways were studied in anesthetized male rats. PVN injections of an α<sub>1</sub>-adrenergic receptor agonist or a serotonergic 5-HT<sub>1A</sub> receptor agonist markedly increased both adrenocorticotropin (ACTH) and corticosterone (CS) serum levels. These responses were significantly inhibited by separate pre-injection of the selective non-NMDA and NMDA glutamate receptor subtype antagonists into the PVN in a dose-dependent manner. Electrical stimulation of either the ventral noradrenergic bundle or the dorsal raphe nucleus markedly increased serum ACTH and CS. These responses were also significantly attenuated by pre-injection of the above glutamate ionotropic receptor antagonists in a dose-dependent manner. These results suggest that glutamatergic interneurons in the PVN, acting via non-NMDA and NMDA receptors, may act as an excitatory mechanism in the NE and 5-HT control of hypothalamic ACTH secretagogues.

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          Most cited references 12

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          Expression of ionotropic glutamate receptor subunit mRNAs by paraventricular corticotropin-releasing factor (CRF) neurons.

          To determine whether paraventricular corticotropin-releasing factor (CRF) neurons express NMDA, AMPA or kainate-preferring glutamate receptors, we have colocalized, by in situ hybridization (ISH), transcripts of various glutamate receptor subunit genes with the CRF messenger RNA on doublet adjacent sections of the rat hypothalamus. We found that more than 70% of CRF-positive neurons contain the NMDA receptor subunit NR1 mRNA whereas NR2A and NR2B subunit mRNAs were not detectable in CRF cells. A significant proportion of identified CRF cells express AMPA receptor subunit GluRA (46%), GluRB (21%) as well as the kainate-preferring receptor subunit KA2 (31%) mRNAs. These results support the hypothesis that the excitatory transmitter glutamate may directly influence CRF neurons through NMDA as well as non-NMDA receptors.
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            Serotonin stimulates corticotropin-releasing factor gene expression in the hypothalamic paraventricular nucleus of conscious rats.

            To examine the direct effects of serotonin (5-HT) on the release and synthesis of corticotropin-releasing factor (CRF) in the hypothalamic paraventricular nucleus (PVN), 5-HT was microinjected just onto the bilateral PVN of conscious rats. Plasma adrenocorticotropic hormone (ACTH) levels peaked at 30 min and returned to the basal levels in 90 min. Northern blot analysis revealed that the CRF messenger RNA (mRNA) level in the PVN as well as the proopiomelanocortin mRNA level in the anterior pituitary significantly increased 120 min after the 5-HT injections (50-250 nmol/side). Pretreatment with intracerebroventricular (i.c.v.) injection of pindobind 5-HT1A (5 nmol) or LY-278584 (500 nmol) completely abolished the 5-HT-induced ACTH response, whereas LY-53857 (100 nmol) was without effect. These results suggest that 5-HT stimulates CRF release, which has interactions with 5-HT1A and 5-HT3 receptors on CRF neurons in the PVN, and activates CRF synthesis in conscious rats.
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              Biochemical evidence for the regulation of central noradrenergic activity by 5-HT1A and 5-HT2 receptors: Microdialysis studies in the awake and anaesthetized rat

               C.J.G. Done,  T Sharp (1994)
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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 2004
                02 February 2004
                : 79
                : 1
                : 43-53
                Affiliations
                Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah University Hospital and Hebrew University-Hadassah Medical School, Jerusalem, Israel
                Article
                76044 Neuroendocrinology 2004;79:43–53
                10.1159/000076044
                14755133
                © 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, References: 49, Pages: 11
                Categories
                Stress and Corticotropin Regulation

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