GAEAA receptor complex function in frontal cortex membranes from control and neurological patients
Identifieur interne : 002B32 ( Main/Corpus ); précédent : 002B31; suivant : 002B33GAEAA receptor complex function in frontal cortex membranes from control and neurological patients
Auteurs : G. Kenneth Lloyd ; Armand Lowenthal ; France Javoy-Agid ; Jean ConstantidinisSource :
- European Journal of Pharmacology [ 0014-2999 ] ; 1991.
Abstract
The functional integrity of the GABAA receptof-benzodiazepine (BZ) recognition site-Cl− ionophore complex was assessed by means of [35S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (n = 4), Alzheimer (n = 7), Parkinson (n = 3) and Huntington's chorea (n = 2) patients. Specific [35S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P < 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABAA receptor-linked Cl− ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [35S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ1 selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [35S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. These studies demonstrate the functional integrity of the GABAA receptor macromolecular complex and also the usefulness of [35S]TBPS binding in the study of human postmortem tissue.
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DOI: 10.1016/0014-2999(91)90361-S
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Kenneth Lloyd</name><affiliation><mods:affiliation>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Lowenthal, Armand" sort="Lowenthal, Armand" uniqKey="Lowenthal A" first="Armand" last="Lowenthal">Armand Lowenthal</name><affiliation><mods:affiliation>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Javoy Agid, France" sort="Javoy Agid, France" uniqKey="Javoy Agid F" first="France" last="Javoy-Agid">France Javoy-Agid</name><affiliation><mods:affiliation>Hopital Pitié Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Constantidinis, Jean" sort="Constantidinis, Jean" uniqKey="Constantidinis J" first="Jean" last="Constantidinis">Jean Constantidinis</name><affiliation><mods:affiliation>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0A9C64FDFDDE488FB659612ABFEB2E432F72039D</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/0014-2999(91)90361-S</idno><idno type="url">https://api.istex.fr/document/0A9C64FDFDDE488FB659612ABFEB2E432F72039D/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002B32</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">GAEAA receptor complex function in frontal cortex membranes from control and neurological patients</title><author><name sortKey="Lloyd, G Kenneth" sort="Lloyd, G Kenneth" uniqKey="Lloyd G" first="G. 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Kenneth Lloyd</name><affiliation><mods:affiliation>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Lowenthal, Armand" sort="Lowenthal, Armand" uniqKey="Lowenthal A" first="Armand" last="Lowenthal">Armand Lowenthal</name><affiliation><mods:affiliation>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Javoy Agid, France" sort="Javoy Agid, France" uniqKey="Javoy Agid F" first="France" last="Javoy-Agid">France Javoy-Agid</name><affiliation><mods:affiliation>Hopital Pitié Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Constantidinis, Jean" sort="Constantidinis, Jean" uniqKey="Constantidinis J" first="Jean" last="Constantidinis">Jean Constantidinis</name><affiliation><mods:affiliation>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Pharmacology</title><title level="j" type="abbrev">EJP</title><idno type="ISSN">0014-2999</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">197</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="33">33</biblScope><biblScope unit="page" to="39">39</biblScope></imprint><idno type="ISSN">0014-2999</idno></series><idno type="istex">0A9C64FDFDDE488FB659612ABFEB2E432F72039D</idno><idno type="DOI">10.1016/0014-2999(91)90361-S</idno><idno type="PII">0014-2999(91)90361-S</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2999</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The functional integrity of the GABAA receptof-benzodiazepine (BZ) recognition site-Cl− ionophore complex was assessed by means of [35S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (n = 4), Alzheimer (n = 7), Parkinson (n = 3) and Huntington's chorea (n = 2) patients. Specific [35S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P < 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABAA receptor-linked Cl− ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [35S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ1 selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [35S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. These studies demonstrate the functional integrity of the GABAA receptor macromolecular complex and also the usefulness of [35S]TBPS binding in the study of human postmortem tissue.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>G.Kenneth Lloyd</name><affiliations><json:string>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Armand Lowenthal</name><affiliations><json:string>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</json:string></affiliations></json:item><json:item><name>France Javoy-Agid</name><affiliations><json:string>Hopital Pitié Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Jean Constantidinis</name><affiliations><json:string>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>GABAA receptor complex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Frontal cortex (human)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>[35S]TBPS binding</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Huntington's chorea</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The functional integrity of the GABAA receptof-benzodiazepine (BZ) recognition site-Cl− ionophore complex was assessed by means of [35S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (n = 4), Alzheimer (n = 7), Parkinson (n = 3) and Huntington's chorea (n = 2) patients. Specific [35S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P > 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABAA receptor-linked Cl− ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [35S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ1 selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [35S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. 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Lloyd, Wyeth Laboratories, Huntercombe Lane South, Taplow, Maidenhead, Berkshire SL6 0PH, U.K..</p></note><affiliation>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Armand</forename><surname>Lowenthal</surname></persName><affiliation>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</affiliation></author><author><persName><forename type="first">France</forename><surname>Javoy-Agid</surname></persName><affiliation>Hopital Pitié Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Jean</forename><surname>Constantidinis</surname></persName><affiliation>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</affiliation></author></analytic><monogr><title level="j">European Journal of Pharmacology</title><title level="j" type="abbrev">EJP</title><idno type="pISSN">0014-2999</idno><idno type="PII">S0014-2999(00)X0863-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991"></date><biblScope unit="volume">197</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="33">33</biblScope><biblScope unit="page" to="39">39</biblScope></imprint></monogr><idno type="istex">0A9C64FDFDDE488FB659612ABFEB2E432F72039D</idno><idno type="DOI">10.1016/0014-2999(91)90361-S</idno><idno type="PII">0014-2999(91)90361-S</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1991</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The functional integrity of the GABAA receptof-benzodiazepine (BZ) recognition site-Cl− ionophore complex was assessed by means of [35S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (n = 4), Alzheimer (n = 7), Parkinson (n = 3) and Huntington's chorea (n = 2) patients. Specific [35S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P < 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABAA receptor-linked Cl− ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [35S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ1 selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [35S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. These studies demonstrate the functional integrity of the GABAA receptor macromolecular complex and also the usefulness of [35S]TBPS binding in the study of human postmortem tissue.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>GABAA receptor complex</term></item><item><term>Frontal cortex (human)</term></item><item><term>[35S]TBPS binding</term></item><item><term>Alzheimer's dementia</term></item><item><term>Parkinson's disease</term></item><item><term>Huntington's chorea</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991-02-05">Registration</change><change when="1991">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></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="fla"><item-info><jid>EJP</jid><aid>9190361S</aid><ce:pii>0014-2999(91)90361-S</ce:pii><ce:doi>10.1016/0014-2999(91)90361-S</ce:doi><ce:copyright type="unknown" year="1991"></ce:copyright></item-info><head><ce:title>GAEA<ce:inf>A</ce:inf> receptor complex function in frontal cortex membranes from control and neurological patients</ce:title><ce:author-group><ce:author><ce:given-name>G.Kenneth</ce:given-name><ce:surname>Lloyd</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Armand</ce:given-name><ce:surname>Lowenthal</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>France</ce:given-name><ce:surname>Javoy-Agid</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jean</ce:given-name><ce:surname>Constantidinis</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>4</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>1</ce:label><ce:textfn>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>2</ce:label><ce:textfn>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>3</ce:label><ce:textfn>Hopital Pitié Salpêtrière, 75013 Paris, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>4</ce:label><ce:textfn>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Correspondence to: G.K. Lloyd, Wyeth Laboratories, Huntercombe Lane South, Taplow, Maidenhead, Berkshire SL6 0PH, U.K..</ce:text></ce:correspondence></ce:author-group><ce:date-received day="23" month="1" year="1991"></ce:date-received><ce:date-accepted day="5" month="2" year="1991"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The functional integrity of the GABA<ce:inf>A</ce:inf> receptof-benzodiazepine (BZ) recognition site-Cl<ce:sup>−</ce:sup> ionophore complex was assessed by means of [<ce:sup loc="pre">35</ce:sup>S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (<ce:italic>n</ce:italic> = 4), Alzheimer (<ce:italic>n</ce:italic> = 7), Parkinson (<ce:italic>n</ce:italic> = 3) and Huntington's chorea (<ce:italic>n</ce:italic> = 2) patients. Specific [<ce:sup loc="pre">35</ce:sup>S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P < 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABA<ce:inf>A</ce:inf> receptor-linked Cl<ce:sup>−</ce:sup> ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [<ce:sup loc="pre">35</ce:sup>S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ<ce:inf>1</ce:inf> selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [<ce:sup loc="pre">35</ce:sup>S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. These studies demonstrate the functional integrity of the GABA<ce:inf>A</ce:inf> receptor macromolecular complex and also the usefulness of [<ce:sup loc="pre">35</ce:sup>S]TBPS binding in the study of human postmortem tissue.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>GABA<ce:inf>A</ce:inf> receptor complex</ce:text></ce:keyword><ce:keyword><ce:text>Frontal cortex (human)</ce:text></ce:keyword><ce:keyword><ce:text>[<ce:sup loc="pre">35</ce:sup>S]TBPS binding</ce:text></ce:keyword><ce:keyword><ce:text>Alzheimer's dementia</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Huntington's chorea</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>GAEAA receptor complex function in frontal cortex membranes from control and neurological patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>GAEA</title></titleInfo><name type="personal"><namePart type="given">G.Kenneth</namePart><namePart type="family">Lloyd</namePart><affiliation>Synlhélabo Recherche (L.E.R.S.), 58 Rue de la Glaciere, 75013 Paris, France</affiliation><description>Correspondence to: G.K. Lloyd, Wyeth Laboratories, Huntercombe Lane South, Taplow, Maidenhead, Berkshire SL6 0PH, U.K..</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Armand</namePart><namePart type="family">Lowenthal</namePart><affiliation>Algemeen Ziekenhuis Middleheim, 2020 Antwerpen, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">France</namePart><namePart type="family">Javoy-Agid</namePart><affiliation>Hopital Pitié Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean</namePart><namePart type="family">Constantidinis</namePart><affiliation>Institutions Universitaires de Psychiatrie Genève (IUPG), 1225 Chène Bourg, Geneva, Switzerland</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">1991</dateIssued><dateValid encoding="w3cdtf">1991-02-05</dateValid><copyrightDate encoding="w3cdtf">1991</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">The functional integrity of the GABAA receptof-benzodiazepine (BZ) recognition site-Cl− ionophore complex was assessed by means of [35S]TBPS (t-butylbicyclophosphorothionate) binding to frontal cortex membranes prepared from frozen postmortem brain tissue taken from control (n = 4), Alzheimer (n = 7), Parkinson (n = 3) and Huntington's chorea (n = 2) patients. Specific [35S]TBPS binding was similar in control, Parkinson's disease and Huntington's chorea brains, but was significantly reduced (78% control, P < 0.01) in frontal cortex membranes from Alzheimer's patients. The linkage between the BZ recognition sites and the GABAA receptor-linked Cl− ionophore was functionally intact in these membranes as BZ site agonists (zolpidem, alpidem, flunitrazepam and clonazepam) enhanced [35S]TBPS binding under the conditions used (well-washed membranes in the presence of 1.0 M NaCl). Zolpidem (BZ1 selective) exhibited a biphasic enhancement in control membranes whereas the other compounds induced a bell-shaped concentration-response curve. The enhancement of [35S]TBPS binding by alpidem, flunitrazepam and clonazepam was greater in frontal cortex membranes from Alzheimer's patients than in controls whereas it tended to be reduced in membranes from the brains of Huntington's chorea patients. These studies demonstrate the functional integrity of the GABAA receptor macromolecular complex and also the usefulness of [35S]TBPS binding in the study of human postmortem tissue.</abstract><subject><genre>Keywords</genre><topic>GABAA receptor complex</topic><topic>Frontal cortex (human)</topic><topic>[35S]TBPS binding</topic><topic>Alzheimer's dementia</topic><topic>Parkinson's disease</topic><topic>Huntington's chorea</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Pharmacology</title></titleInfo><titleInfo type="abbreviated"><title>EJP</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19910502</dateIssued></originInfo><identifier type="ISSN">0014-2999</identifier><identifier type="PII">S0014-2999(00)X0863-1</identifier><part><date>19910502</date><detail type="volume"><number>197</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>116</end></extent><extent unit="pages"><start>33</start><end>39</end></extent></part></relatedItem><identifier type="istex">0A9C64FDFDDE488FB659612ABFEB2E432F72039D</identifier><identifier type="DOI">10.1016/0014-2999(91)90361-S</identifier><identifier type="PII">0014-2999(91)90361-S</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/0A9C64FDFDDE488FB659612ABFEB2E432F72039D/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">PHARMACOLOGY & PHARMACY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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