Melatonin: A Clock‐Output, A Clock‐Input
Identifieur interne : 000929 ( Main/Corpus ); précédent : 000928; suivant : 000930Melatonin: A Clock‐Output, A Clock‐Input
Auteurs : J. H. Stehle ; C. Von Gall ; H. KorfSource :
- Journal of Neuroendocrinology [ 0953-8194 ] ; 2003-04.
English descriptors
- KwdEn :
Abstract
In mammals, the circadian system is comprised of three major components: the lateral eyes, the hypothalamic suprachiasmatic nucleus (SCN) and the pineal gland. The SCN harbours the endogenous oscillator that is entrained every day to the ambient lighting conditions via retinal input. Among the many circadian rhythms in the body that are driven by SCN output, the synthesis of melatonin in the pineal gland functions as a hormonal message encoding for the duration of darkness. Dissemination of this circadian information relies on the activation of melatonin receptors, which are most prominently expressed in the SCN, and the hypophyseal pars tuberalis (PT), but also in many other tissues. A deficiency in melatonin, or a lack in melatonin receptors should therefore have effects on circadian biology. However, our investigations of mice that are melatonin‐proficient with mice that do not make melatonin, or alternatively cannot interpret the melatonin message, revealed that melatonin has only minor effects on signal transduction processes within the SCN and sets, at most, the gain for clock error signals mediated via the retino‐hypothalamic tract. Melatonin deficiency has no effect on the rhythm generation, or on the maintenance of the oscillation. By contrast, melatonin is essential for rhythmic signalling in the PT. Here, melatonin acts in concert with adenosine to elicit rhythms in clock gene expression. By sensitizing adenylyl cyclase, melatonin opens a temporally‐restricted gate and thus lowers the threshold for adenosine to induce cAMP‐sensitive genes. This interaction, which determines a temporally precise regulation of gene expression, and by endocrine–endocrine interactions possibly also pituitary output, may reflect a general mechanism by which the master clock in the brain synchronizes clock cells in peripheral tissues that require unique phasing of output signals.
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DOI: 10.1046/j.1365-2826.2003.01001.x
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ISTEX:404AD2392AC6B2D66D5BCC06A8805BFADB17346ALe document en format XML
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The SCN harbours the endogenous oscillator that is entrained every day to the ambient lighting conditions via retinal input. Among the many circadian rhythms in the body that are driven by SCN output, the synthesis of melatonin in the pineal gland functions as a hormonal message encoding for the duration of darkness. Dissemination of this circadian information relies on the activation of melatonin receptors, which are most prominently expressed in the SCN, and the hypophyseal pars tuberalis (PT), but also in many other tissues. A deficiency in melatonin, or a lack in melatonin receptors should therefore have effects on circadian biology. However, our investigations of mice that are melatonin‐proficient with mice that do not make melatonin, or alternatively cannot interpret the melatonin message, revealed that melatonin has only minor effects on signal transduction processes within the SCN and sets, at most, the gain for clock error signals mediated via the retino‐hypothalamic tract. Melatonin deficiency has no effect on the rhythm generation, or on the maintenance of the oscillation. By contrast, melatonin is essential for rhythmic signalling in the PT. Here, melatonin acts in concert with adenosine to elicit rhythms in clock gene expression. By sensitizing adenylyl cyclase, melatonin opens a temporally‐restricted gate and thus lowers the threshold for adenosine to induce cAMP‐sensitive genes. This interaction, which determines a temporally precise regulation of gene expression, and by endocrine–endocrine interactions possibly also pituitary output, may reflect a general mechanism by which the master clock in the brain synchronizes clock cells in peripheral tissues that require unique phasing of output signals.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>J. H. 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H.</forename><surname>Stehle</surname></persName><affiliation>Institute of Anatomy II, Johann Wolfgang Goethe‐University Frankfurt, Frankfurt, Germany.</affiliation></author><author><persName><forename type="first">C.</forename><surname>Von Gall</surname></persName><affiliation>Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA, USA.</affiliation></author><author><persName><forename type="first">H.‐W.</forename><surname>Korf</surname></persName><affiliation>Institute of Anatomy II, Johann Wolfgang Goethe‐University Frankfurt, Frankfurt, Germany.</affiliation></author></analytic><monogr><title level="j">Journal of Neuroendocrinology</title><idno type="pISSN">0953-8194</idno><idno type="eISSN">1365-2826</idno><idno type="DOI">10.1111/(ISSN)1365-2826</idno><imprint><publisher>Blackwell Science, Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-04"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="383">383</biblScope><biblScope unit="page" to="389">389</biblScope></imprint></monogr><idno type="istex">404AD2392AC6B2D66D5BCC06A8805BFADB17346A</idno><idno type="DOI">10.1046/j.1365-2826.2003.01001.x</idno><idno type="ArticleID">JNE1001</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In mammals, the circadian system is comprised of three major components: the lateral eyes, the hypothalamic suprachiasmatic nucleus (SCN) and the pineal gland. 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Melatonin deficiency has no effect on the rhythm generation, or on the maintenance of the oscillation. By contrast, melatonin is essential for rhythmic signalling in the PT. Here, melatonin acts in concert with adenosine to elicit rhythms in clock gene expression. By sensitizing adenylyl cyclase, melatonin opens a temporally‐restricted gate and thus lowers the threshold for adenosine to induce cAMP‐sensitive genes. 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Stehle, Dr Senckenbergische Anatomie, Institute of Anatomy II, Johann Wolfgang Goethe‐Universität Frankfurt, Theodor‐Stern‐Kai 7, D‐60590 Frankfurt, Germany (e‐mail: <email normalForm="stehle@em.uni-frankfurt.de">stehle@em.uni‐frankfurt.de</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JNE.JNE1001.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="40"></count><count type="wordTotal" number="5686"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Melatonin: A Clock‐Output, A Clock‐Input</title><title type="short">Clock‐output, clock‐input</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>J. H.</givenNames><familyName>Stehle</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>C.</givenNames><familyName>Von Gall</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>H.‐W.</givenNames><familyName>Korf</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation> Institute of Anatomy II, Johann Wolfgang Goethe‐University Frankfurt, Frankfurt, Germany.
</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA, USA.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">pineal</keyword><keyword xml:id="k2">suprachiasmatic nucleus</keyword><keyword xml:id="k3">pars tuberalis</keyword><keyword xml:id="k4">melatonin</keyword><keyword xml:id="k5">cylicAMP signalling</keyword><keyword xml:id="k6">clock genes</keyword><keyword xml:id="k7">period</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In mammals, the circadian system is comprised of three major components: the lateral eyes, the hypothalamic suprachiasmatic nucleus (SCN) and the pineal gland. The SCN harbours the endogenous oscillator that is entrained every day to the ambient lighting conditions via retinal input. 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The SCN harbours the endogenous oscillator that is entrained every day to the ambient lighting conditions via retinal input. Among the many circadian rhythms in the body that are driven by SCN output, the synthesis of melatonin in the pineal gland functions as a hormonal message encoding for the duration of darkness. Dissemination of this circadian information relies on the activation of melatonin receptors, which are most prominently expressed in the SCN, and the hypophyseal pars tuberalis (PT), but also in many other tissues. A deficiency in melatonin, or a lack in melatonin receptors should therefore have effects on circadian biology. However, our investigations of mice that are melatonin‐proficient with mice that do not make melatonin, or alternatively cannot interpret the melatonin message, revealed that melatonin has only minor effects on signal transduction processes within the SCN and sets, at most, the gain for clock error signals mediated via the retino‐hypothalamic tract. Melatonin deficiency has no effect on the rhythm generation, or on the maintenance of the oscillation. By contrast, melatonin is essential for rhythmic signalling in the PT. Here, melatonin acts in concert with adenosine to elicit rhythms in clock gene expression. By sensitizing adenylyl cyclase, melatonin opens a temporally‐restricted gate and thus lowers the threshold for adenosine to induce cAMP‐sensitive genes. 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