In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone
Identifieur interne : 000663 ( Istex/Corpus ); précédent : 000662; suivant : 000664In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone
Auteurs : Patricia A. BroderickSource :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1991.
English descriptors
- Teeft :
- Accumbens, Accumbens synaptic concentrations, Animal control values, Anova, Basal, Baseline values, Brain dopamine, Broderick, Cocaine, Cocaine administration, Cocaine effects, Differential effects, Dopamine, Dopamine metabolites, Electrochemical, Experimental studies, Extracellular dopamine, Impulse flow, Impulse flow block, Impulse flow inhibition, Impulse flow inhibitor, Levels postmortem, Neuron, Neuronal, Neuronal impulse flow, Nucleus accumbens, Pharmacol, Presynaptic, Presynaptic mechanisms, Release mechanism, Release mechanisms, Reuptake inhibition, Rhesus monkeys, Same animal control, Serotonin, Spike discharges, Surgical procedure, Synaptic, Synaptic concentrations, Synaptie concentrations, Unrestrained, Uptake inhibition, Vivo, Vivo electrochemical, Vivo electrochemical signal, Vivo electrochemical signals, Vivo voltammetric, Vivo voltammetric studies, Vivo voltammetry, Voltammetric.
Abstract
Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.
Url:
DOI: 10.1016/0091-3057(91)90113-G
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ISTEX:487D1EEA4A668F35C2536348CE9A38E558A0FC59Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</title><author><name sortKey="Broderick, Patricia A" sort="Broderick, Patricia A" uniqKey="Broderick P" first="Patricia A." last="Broderick">Patricia A. Broderick</name><affiliation><mods:affiliation>Department of Pharmacology, Room J-910, The City University of New York Medical School, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:487D1EEA4A668F35C2536348CE9A38E558A0FC59</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/0091-3057(91)90113-G</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-C87ZD6TK-Q/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000663</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000663</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</title><author><name sortKey="Broderick, Patricia A" sort="Broderick, Patricia A" uniqKey="Broderick P" first="Patricia A." last="Broderick">Patricia A. Broderick</name><affiliation><mods:affiliation>Department of Pharmacology, Room J-910, The City University of New York Medical School, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Pharmacology, Biochemistry and Behavior</title><title level="j" type="abbrev">PBB</title><idno type="ISSN">0091-3057</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">40</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="969">969</biblScope><biblScope unit="page" to="975">975</biblScope></imprint><idno type="ISSN">0091-3057</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0091-3057</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Accumbens</term><term>Accumbens synaptic concentrations</term><term>Animal control values</term><term>Anova</term><term>Basal</term><term>Baseline values</term><term>Brain dopamine</term><term>Broderick</term><term>Cocaine</term><term>Cocaine administration</term><term>Cocaine effects</term><term>Differential effects</term><term>Dopamine</term><term>Dopamine metabolites</term><term>Electrochemical</term><term>Experimental studies</term><term>Extracellular dopamine</term><term>Impulse flow</term><term>Impulse flow block</term><term>Impulse flow inhibition</term><term>Impulse flow inhibitor</term><term>Levels postmortem</term><term>Neuron</term><term>Neuronal</term><term>Neuronal impulse flow</term><term>Nucleus accumbens</term><term>Pharmacol</term><term>Presynaptic</term><term>Presynaptic mechanisms</term><term>Release mechanism</term><term>Release mechanisms</term><term>Reuptake inhibition</term><term>Rhesus monkeys</term><term>Same animal control</term><term>Serotonin</term><term>Spike discharges</term><term>Surgical procedure</term><term>Synaptic</term><term>Synaptic concentrations</term><term>Synaptie concentrations</term><term>Unrestrained</term><term>Uptake inhibition</term><term>Vivo</term><term>Vivo electrochemical</term><term>Vivo electrochemical signal</term><term>Vivo electrochemical signals</term><term>Vivo voltammetric</term><term>Vivo voltammetric studies</term><term>Vivo voltammetry</term><term>Voltammetric</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>cocaine</json:string><json:string>accumbens</json:string><json:string>synaptic</json:string><json:string>dopamine</json:string><json:string>synaptic concentrations</json:string><json:string>nucleus accumbens</json:string><json:string>electrochemical</json:string><json:string>pharmacol</json:string><json:string>anova</json:string><json:string>serotonin</json:string><json:string>unrestrained</json:string><json:string>broderick</json:string><json:string>basal</json:string><json:string>impulse flow</json:string><json:string>voltammetric</json:string><json:string>presynaptic</json:string><json:string>cocaine administration</json:string><json:string>release mechanisms</json:string><json:string>vivo electrochemical</json:string><json:string>impulse flow block</json:string><json:string>neuronal impulse flow</json:string><json:string>impulse flow inhibition</json:string><json:string>vivo voltammetric studies</json:string><json:string>vivo voltammetry</json:string><json:string>neuron</json:string><json:string>neuronal</json:string><json:string>vivo</json:string><json:string>impulse flow inhibitor</json:string><json:string>brain dopamine</json:string><json:string>vivo electrochemical signal</json:string><json:string>vivo electrochemical signals</json:string><json:string>animal control values</json:string><json:string>baseline values</json:string><json:string>experimental studies</json:string><json:string>synaptie concentrations</json:string><json:string>same animal control</json:string><json:string>dopamine metabolites</json:string><json:string>spike discharges</json:string><json:string>reuptake inhibition</json:string><json:string>vivo voltammetric</json:string><json:string>accumbens synaptic concentrations</json:string><json:string>surgical procedure</json:string><json:string>cocaine effects</json:string><json:string>levels postmortem</json:string><json:string>release mechanism</json:string><json:string>presynaptic mechanisms</json:string><json:string>rhesus monkeys</json:string><json:string>extracellular dopamine</json:string><json:string>uptake inhibition</json:string><json:string>differential effects</json:string></teeft></keywords><author><json:item><name>Patricia A. Broderick</name><affiliations><json:string>Department of Pharmacology, Room J-910, The City University of New York Medical School, USA</json:string><json:string>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Cocaine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Gamma-butyrolactone (γ-BL)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Nucleus accumbens</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Freely moving rat</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>In vivo electrochemistry (voltammetry)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Presynaptic release</value></json:item></subject><arkIstex>ark:/67375/6H6-C87ZD6TK-Q</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Short communication</json:string></originalGenre><abstract>Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p>0.0001) after DA impulse flow was significantly inhibited (p>0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p>0.0004) after impulse flow was significantly inhibited (p>0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</abstract><qualityIndicators><score>8.242</score><pdfWordCount>4058</pdfWordCount><pdfCharCount>25546</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>605 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>182</abstractWordCount><abstractCharCount>1255</abstractCharCount><keywordCount>8</keywordCount></qualityIndicators><title>In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</title><pmid><json:string>1816583</json:string></pmid><pii><json:string>0091-3057(91)90113-G</json:string></pii><genre><json:string>brief-communication</json:string></genre><serie><title>Cocaine and other stimulants. Advances in behavioral biology</title><language><json:string>unknown</json:string></language><volume>vol. 21</volume><pages><first>373</first><last>407</last></pages></serie><host><title>Pharmacology, Biochemistry and Behavior</title><language><json:string>unknown</json:string></language><publicationDate>1991</publicationDate><issn><json:string>0091-3057</json:string></issn><pii><json:string>S0091-3057(00)X0325-5</json:string></pii><volume>40</volume><issue>4</issue><pages><first>969</first><last>975</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1991</json:string></date><geogName></geogName><orgName><json:string>The City University</json:string><json:string>Becker Parkin Dental Supply Co.</json:string><json:string>Fisher Scientific</json:string><json:string>American Hospital Supply, Edison</json:string><json:string>NIDA Award</json:string></orgName><orgName_funder><json:string>NIDA Award</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Robert Wechsler</json:string><json:string>Frank Phelan</json:string><json:string>P. 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The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Cocaine</term></item><item><term>Gamma-butyrolactone (γ-BL)</term></item><item><term>Dopamine</term></item><item><term>Serotonin</term></item><item><term>Nucleus accumbens</term></item><item><term>Freely moving rat</term></item><item><term>In vivo electrochemistry (voltammetry)</term></item><item><term>Presynaptic release</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-C87ZD6TK-Q/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="sco"><item-info><jid>PBB</jid><aid>9190113G</aid><ce:pii>0091-3057(91)90113-G</ce:pii><ce:doi>10.1016/0091-3057(91)90113-G</ce:doi><ce:copyright type="unknown" year="1991"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Rapid communication</ce:textfn></ce:dochead><ce:title>In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</ce:title><ce:author-group><ce:author><ce:given-name>Patricia A.</ce:given-name><ce:surname>Broderick</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Pharmacology, Room J-910, The City University of New York Medical School, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031, USA</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="28" month="8" year="1991"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (<ce:italic>Rattus norvegicus</ce:italic>). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (<ce:italic>p</ce:italic><0.0001) after DA impulse flow was significantly inhibited (<ce:italic>p</ce:italic><0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (<ce:italic>p</ce:italic><0.0004) after impulse flow was significantly inhibited (<ce:italic>p</ce:italic><0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Cocaine</ce:text></ce:keyword><ce:keyword><ce:text>Gamma-butyrolactone (γ-BL)</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>Serotonin</ce:text></ce:keyword><ce:keyword><ce:text>Nucleus accumbens</ce:text></ce:keyword><ce:keyword><ce:text>Freely moving rat</ce:text></ce:keyword><ce:keyword><ce:text>In vivo electrochemistry (voltammetry)</ce:text></ce:keyword><ce:keyword><ce:text>Presynaptic release</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone</title></titleInfo><name type="personal"><namePart type="given">Patricia A.</namePart><namePart type="family">Broderick</namePart><affiliation>Department of Pharmacology, Room J-910, The City University of New York Medical School, USA</affiliation><affiliation>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="Short communication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued><copyrightDate encoding="w3cdtf">1991</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</abstract><note type="content">Section title: Rapid communication</note><subject><genre>Keywords</genre><topic>Cocaine</topic><topic>Gamma-butyrolactone (γ-BL)</topic><topic>Dopamine</topic><topic>Serotonin</topic><topic>Nucleus accumbens</topic><topic>Freely moving rat</topic><topic>In vivo electrochemistry (voltammetry)</topic><topic>Presynaptic release</topic></subject><relatedItem type="host"><titleInfo><title>Pharmacology, Biochemistry and Behavior</title></titleInfo><titleInfo type="abbreviated"><title>PBB</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued></originInfo><identifier type="ISSN">0091-3057</identifier><identifier type="PII">S0091-3057(00)X0325-5</identifier><part><date>1991</date><detail type="volume"><number>40</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue-pages"><start>709</start><end>1058</end></extent><extent unit="pages"><start>969</start><end>975</end></extent></part></relatedItem><identifier type="istex">487D1EEA4A668F35C2536348CE9A38E558A0FC59</identifier><identifier type="ark">ark:/67375/6H6-C87ZD6TK-Q</identifier><identifier type="DOI">10.1016/0091-3057(91)90113-G</identifier><identifier type="PII">0091-3057(91)90113-G</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-C87ZD6TK-Q/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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