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      Circadian Rhythms of Dopamine and Dihydroxyphenyl Acetic Acid in the Mouse Striatum: Effects of Pinealectomy and of Melatonin Treatment

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          Abstract

          The existence of dopamine (DA)-melatonin (aMT) relationships is well documented in several brain areas of the mammalian central nervous system such as the retina and hypothalamus or the nigrostriatal system. For instance, aMT tempers 1 methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigrostriatal damage in C57BL/6 mice. In this mouse strain however, rhythmic production of aMT and its possible interaction with striatal DA is still unclear. In the present work we investigated circadian variations in pineal production of aMT and striatal DA levels in C57BL/6 mice. Effects of pinealectomy and aMT administration were also assessed. Intact, pinealectomized and pinealectomized + aMT-treated mice and their respective control groups were sacrificed at six different times during the 24-hour period. In control animals, aMT displayed a circadian rhythm with a narrow peak at midnight. The peak of aMT coincided with the nadir of the DA rhythm present in the striatum. Shortly after the decrease of DA levels, an increase in 3,4-dihydroxyphenylacetic acid (DOPAC), the main DA metabolite, was observed. The rhythmic changes of DA and DOPAC levels in the striatum were blunted by pinealectomy, whereas administration of aMT (0.1–10 mg/kg) during 6 days to pinealectomized mice restored the rhythms in a dose-dependent manner. Striatal levels of 3-methoxytyramine and homovanillic acid did not change during the 24-hour cycle. The serotonergic system, assessed by the determination of 5-hydroxytryptamine and 5-hydroxyindole-3-acetic acid concentration in striatum, did not show significant time-dependent changes in control animals and was not affected by pinealectomy or aMT treatment. These data substantiate the existence of a link between pineal function, melatonin secretion and DA circadian rhythm in the mouse striatum.

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          Most cited references 12

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          Chemistry, physiology and pathology of free radicals

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            Dopamine inhibits melatonin release in the mammalian retina: in vitro evidence.

            A circadian oscillator located within the retina controls melatonin synthesis in the retina of mammals. In non-mammalian vertebrates retinal melatonin and dopamine appear to act as mutually inhibitory paracrine signals for night and day, respectively; while in mammals this mutually inhibitory capability has now been fully demonstrated. In this study using a flow-through culture apparatus we investigated melatonin release from cultured retinas of golden hamster (Mesocricetus auratus) in the presence of dopamine or dopaminergic agonists and antagonists. Neural retinas were cultured with medium 199 for 24 h in a flow-through apparatus at the temperature 33 degrees C. During the subjective night the culturing medium was supplemented with dopamine, dopamine receptor antagonists or agonists. At the concentration of 0.1 microM dopamine did not inhibit melatonin release, while at higher dopamine concentration (1 to 1000 microM) melatonin release was inhibited in a dose-dependent manner. These effects appeared to be mediated by a D2/D4 receptor, because D2 and D4 receptor agonists (100 microM), but not D1/D5 receptor agonists (100 microM), inhibited melatonin release. Furthermore, D2/D4 selective receptor antagonists (100 microM) in conjunction with 100 microM dopamine blocked melatonin suppression, whereas a D1/D5 selective receptors antagonist was completely ineffective. Taken together, these results directly demonstrate for the first time that in the retina of mammals dopamine may suppress melatonin, and that suppression is mediated by D2/D4 dopaminergic receptors.
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              Enzyme-Dependent Ascorbate Recycling in Human Erythrocytes: Role of Thioredoxin Reductase

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2002
                March 2002
                21 March 2002
                : 75
                : 3
                : 201-208
                Affiliations
                aDepartamento de Fisiología, Instituto de Biotecnología, Universidad de Granada, y bDepartamento de Farmacología y Fisiología, Facultad de Medicina, Universidad de Zaragoza, España
                Article
                48238 Neuroendocrinology 2002;75:201–208
                10.1159/000048238
                11914592
                © 2002 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: 6, References: 54, Pages: 8
                Categories
                Neuroendocrine Regulation of Catecholamine Neurons

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