Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes
Identifieur interne : 001086 ( Istex/Corpus ); précédent : 001085; suivant : 001087Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes
Auteurs : K. M. Pirke ; A. Broocks ; T. Wilckens ; R. Marquard ; U. SchweigerSource :
- Neuroscience and Biobehavioral Reviews [ 0149-7634 ] ; 1993.
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Abstract
Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by α2-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. The observation of the serotonergic system might help to develop a pharmacological treatment of hyperactivity in anorectic patients.
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DOI: 10.1016/S0149-7634(05)80012-0
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ISTEX:0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FDLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</title><author><name sortKey="Pirke, K M" sort="Pirke, K M" uniqKey="Pirke K" first="K. M." last="Pirke">K. M. Pirke</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</mods:affiliation></affiliation></author><author><name sortKey="Broocks, A" sort="Broocks, A" uniqKey="Broocks A" first="A." last="Broocks">A. Broocks</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wilckens, T" sort="Wilckens, T" uniqKey="Wilckens T" first="T." last="Wilckens">T. Wilckens</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Marquard, R" sort="Marquard, R" uniqKey="Marquard R" first="R." last="Marquard">R. Marquard</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schweiger, U" sort="Schweiger, U" uniqKey="Schweiger U" first="U." last="Schweiger">U. 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Pirke</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</mods:affiliation></affiliation></author><author><name sortKey="Broocks, A" sort="Broocks, A" uniqKey="Broocks A" first="A." last="Broocks">A. Broocks</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wilckens, T" sort="Wilckens, T" uniqKey="Wilckens T" first="T." last="Wilckens">T. Wilckens</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Marquard, R" sort="Marquard, R" uniqKey="Marquard R" first="R." last="Marquard">R. Marquard</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schweiger, U" sort="Schweiger, U" uniqKey="Schweiger U" first="U." last="Schweiger">U. Schweiger</name><affiliation><mods:affiliation>Max-Planck-Institute for Psychiatry, Division of Psychoneuroendocrinology, Kraepelinstr. 10, 8000 Munich 40, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuroscience and Biobehavioral Reviews</title><title level="j" type="abbrev">NBR</title><idno type="ISSN">0149-7634</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="287">287</biblScope><biblScope unit="page" to="294">294</biblScope></imprint><idno type="ISSN">0149-7634</idno></series><idno type="istex">0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD</idno><idno type="DOI">10.1016/S0149-7634(05)80012-0</idno><idno type="PII">S0149-7634(05)80012-0</idno><idno type="ArticleID">05800120</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0149-7634</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal model</term><term>Anorexia nervosa</term><term>Corticosterone</term><term>Estrus</term><term>Serotonin</term><term>Testosterone</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by α2-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. The observation of the serotonergic system might help to develop a pharmacological treatment of hyperactivity in anorectic patients.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>K.M. Pirke</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</json:string><json:string>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</json:string></affiliations></json:item><json:item><name>A. Broocks</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</json:string></affiliations></json:item><json:item><name>T. Wilckens</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</json:string></affiliations></json:item><json:item><name>R. Marquard</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</json:string></affiliations></json:item><json:item><name>U. Schweiger</name><affiliations><json:string>Max-Planck-Institute for Psychiatry, Division of Psychoneuroendocrinology, Kraepelinstr. 10, 8000 Munich 40, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Anorexia nervosa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Animal model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Corticosterone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Estrus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Testosterone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serotonin</value></json:item></subject><articleId><json:string>05800120</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by α2-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. 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Behav.</title></host><title>Activation of α2-adrenoceptors suppresses excessive wheel-running in the semistarvation-induced hyperactive rat</title></json:item><json:item><host><author></author></host></json:item></refBibs><genre><json:string>research-article</json:string></genre><serie><language><json:string>unknown</json:string></language><title>Doctoral thesis</title></serie><host><volume>17</volume><pii><json:string>S0149-7634(05)X8009-5</json:string></pii><pages><last>294</last><first>287</first></pages><issn><json:string>0149-7634</json:string></issn><issue>3</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Neuroscience and Biobehavioral Reviews</title><publicationDate>1993</publicationDate></host><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1016/S0149-7634(05)80012-0</json:string></doi><id>0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD</id><score>1.2001647</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1993 Pergamon Press Ltd.</p></availability><date>1993</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</title><author xml:id="author-1"><persName><forename type="first">K.M.</forename><surname>Pirke</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation><affiliation>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</affiliation></author><author xml:id="author-2"><persName><forename type="first">A.</forename><surname>Broocks</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">T.</forename><surname>Wilckens</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">R.</forename><surname>Marquard</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">U.</forename><surname>Schweiger</surname></persName><affiliation>Max-Planck-Institute for Psychiatry, Division of Psychoneuroendocrinology, Kraepelinstr. 10, 8000 Munich 40, Germany</affiliation></author></analytic><monogr><title level="j">Neuroscience and Biobehavioral Reviews</title><title level="j" type="abbrev">NBR</title><idno type="pISSN">0149-7634</idno><idno type="PII">S0149-7634(05)X8009-5</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="287">287</biblScope><biblScope unit="page" to="294">294</biblScope></imprint></monogr><idno type="istex">0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD</idno><idno type="DOI">10.1016/S0149-7634(05)80012-0</idno><idno type="PII">S0149-7634(05)80012-0</idno><idno type="ArticleID">05800120</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by α2-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. The observation of the serotonergic system might help to develop a pharmacological treatment of hyperactivity in anorectic patients.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Anorexia nervosa</term></item><item><term>Animal model</term></item><item><term>Corticosterone</term></item><item><term>Estrus</term></item><item><term>Testosterone</term></item><item><term>Serotonin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="fla"><item-info><jid>NBR</jid><aid>05800120</aid><ce:pii>S0149-7634(05)80012-0</ce:pii><ce:doi>10.1016/S0149-7634(05)80012-0</ce:doi><ce:copyright type="unknown" year="1993">Pergamon Press Ltd.</ce:copyright></item-info><head><ce:title>Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</ce:title><ce:author-group><ce:author><ce:given-name>K.M.</ce:given-name><ce:surname>Pirke</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref><ce:cross-ref refid="cor1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>A.</ce:given-name><ce:surname>Broocks</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>T.</ce:given-name><ce:surname>Wilckens</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>R.</ce:given-name><ce:surname>Marquard</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>U.</ce:given-name><ce:surname>Schweiger</ce:surname><ce:cross-ref refid="aff2">†</ce:cross-ref></ce:author><ce:affiliation id="aff1"><ce:label>*</ce:label><ce:textfn>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</ce:textfn></ce:affiliation><ce:affiliation id="aff2"><ce:label>†</ce:label><ce:textfn>Max-Planck-Institute for Psychiatry, Division of Psychoneuroendocrinology, Kraepelinstr. 10, 8000 Munich 40, Germany</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>1</ce:label><ce:text>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="26" month="8" year="1992"></ce:date-received><ce:abstract id="ab1" class="author" xml:lang="en"><ce:abstract-sec><ce:simple-para>Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by <ce:italic>α</ce:italic><ce:inf loc="post">2</ce:inf>-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. The observation of the serotonergic system might help to develop a pharmacological treatment of hyperactivity in anorectic patients.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Anorexia nervosa</ce:text></ce:keyword><ce:keyword><ce:text>Animal model</ce:text></ce:keyword><ce:keyword><ce:text>Corticosterone</ce:text></ce:keyword><ce:keyword><ce:text>Estrus</ce:text></ce:keyword><ce:keyword><ce:text>Testosterone</ce:text></ce:keyword><ce:keyword><ce:text>Serotonin</ce:text></ce:keyword></ce:keywords></head><tail><ce:bibliography><ce:section-title>References</ce:section-title><ce:bibliography-sec><ce:bib-reference id="bib1"><ce:label>1.</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Bendotti</ce:surname><ce:given-name>C.</ce:given-name></sb:author><sb:author><ce:surname>Samanin</ce:surname><ce:given-name>R.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>The role of putative 5-HT<ce:inf loc="post">1A</ce:inf> and 5-HT<ce:inf loc="post">1B</ce:inf> receptors in the control of feeding in rats</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Life Sci.</sb:maintitle></sb:title><sb:volume-nr>41</sb:volume-nr></sb:series><sb:date>1987</sb:date></sb:issue><sb:pages><sb:first-page>635</sb:first-page><sb:last-page>642</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib2"><ce:label>2.</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Broocks</ce:surname><ce:given-name>A.</ce:given-name></sb:author><sb:author><ce:surname>Liu</ce:surname><ce:given-name>J.</ce:given-name></sb:author><sb:author><ce:surname>Pirke</ce:surname><ce:given-name>K.M.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Influence of hyperativity on the metabolism of central monoaminergic neurotransmitters and reproductive function in the semistarved rat</sb:maintitle></sb:title></sb:contribution><sb:host><sb:edited-book><sb:editors><sb:editor><ce:surname>Pirke</ce:surname><ce:given-name>K.M.</ce:given-name></sb:editor><sb:editor><ce:surname>Wuttke</ce:surname><ce:given-name>W.</ce:given-name></sb:editor><sb:editor><ce:surname>Schweiger</ce:surname><ce:given-name>U.</ce:given-name></sb:editor></sb:editors><sb:title><sb:maintitle>The menstrual cycle and its disorder</sb:maintitle></sb:title><sb:date>1989</sb:date><sb:publisher><sb:name>Springer-Verlag</sb:name><sb:location>Berlin</sb:location></sb:publisher></sb:edited-book><sb:pages><sb:first-page>88</sb:first-page><sb:last-page>96</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib3"><ce:label>3.</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Broocks</ce:surname><ce:given-name>A.</ce:given-name></sb:author><sb:author><ce:surname>Liu</ce:surname><ce:given-name>J.</ce:given-name></sb:author><sb:author><ce:surname>Pirke</ce:surname><ce:given-name>K.M.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Semistarvation-induced hyperactivity compensates for decreased norepinephrine and dopamine turnover in the mediobasal hypothalamus of the rat</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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Psychopharmacology 100:417–425.</ce:textref></ce:other-ref></ce:bib-reference></ce:bibliography-sec></ce:bibliography></tail></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes</title></titleInfo><name type="personal"><namePart type="given">K.M.</namePart><namePart type="family">Pirke</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation><affiliation>Requests for reprints should be addressed to K.M. Pirke, Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Broocks</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Wilckens</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Marquard</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, Department of Psychoendocrinology, University of Trier, Building D, Box 3825, 5500 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U.</namePart><namePart type="family">Schweiger</namePart><affiliation>Max-Planck-Institute for Psychiatry, Division of Psychoneuroendocrinology, Kraepelinstr. 10, 8000 Munich 40, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Semistarved rats develop high running wheel activity. This running activity induces increased norepinephrine, dopamine, and serotonin turnover in the hypothalamus. Corticosterone in plasma becomes increased while luteinizing hormone and testosterone are suppressed. In female rats cyclic gonadal function is suppressed. Running activity in the semistarved rats can be suppressed specifically by serotonin 1-c-agonists and by α2-adrenoceptor agonists. This animal model is helpful in the understanding of the combined effects of starvation and hyperactivity, which are observed in many patients with anorexia nervosa. The observation of the serotonergic system might help to develop a pharmacological treatment of hyperactivity in anorectic patients.</abstract><subject lang="en"><genre>Keywords</genre><topic>Anorexia nervosa</topic><topic>Animal model</topic><topic>Corticosterone</topic><topic>Estrus</topic><topic>Testosterone</topic><topic>Serotonin</topic></subject><relatedItem type="host"><titleInfo><title>Neuroscience and Biobehavioral Reviews</title></titleInfo><titleInfo type="abbreviated"><title>NBR</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199323</dateIssued></originInfo><identifier type="ISSN">0149-7634</identifier><identifier type="PII">S0149-7634(05)X8009-5</identifier><part><date>199323</date><detail type="volume"><number>17</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue pages"><start>237</start><end>357</end></extent><extent unit="pages"><start>287</start><end>294</end></extent></part></relatedItem><identifier type="istex">0FE58D2BC76E27E5AB2A3C55BFF928D66923B2FD</identifier><identifier type="DOI">10.1016/S0149-7634(05)80012-0</identifier><identifier type="PII">S0149-7634(05)80012-0</identifier><identifier type="ArticleID">05800120</identifier><accessCondition type="use and reproduction" contentType="copyright">©1993 Pergamon Press Ltd.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Pergamon Press Ltd., ©1993</recordOrigin></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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