Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats
Identifieur interne : 001855 ( Istex/Corpus ); précédent : 001854; suivant : 001856Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats
Auteurs : D. N. Abrous ; J. M. Rivet ; M. Le Moal ; J. P. HermanSource :
- Brain Research [ 0006-8993 ] ; 1990.
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Abstract
Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.
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DOI: 10.1016/0006-8993(90)91221-2
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title><author><name sortKey="Abrous, D N" sort="Abrous, D N" uniqKey="Abrous D" first="D. N." last="Abrous">D. N. Abrous</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Rivet, J M" sort="Rivet, J M" uniqKey="Rivet J" first="J. M." last="Rivet">J. M. Rivet</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Le Moal, M" sort="Le Moal, M" uniqKey="Le Moal M" first="M." last="Le Moal">M. Le Moal</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Herman, J P" sort="Herman, J P" uniqKey="Herman J" first="J. P." last="Herman">J. P. Herman</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4EFCEB24B6BC20CF15B09933429C849E063885A9</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1016/0006-8993(90)91221-2</idno><idno type="url">https://api.istex.fr/document/4EFCEB24B6BC20CF15B09933429C849E063885A9/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001855</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001855</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title><author><name sortKey="Abrous, D N" sort="Abrous, D N" uniqKey="Abrous D" first="D. N." last="Abrous">D. N. Abrous</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Rivet, J M" sort="Rivet, J M" uniqKey="Rivet J" first="J. M." last="Rivet">J. M. Rivet</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Le Moal, M" sort="Le Moal, M" uniqKey="Le Moal M" first="M." last="Le Moal">M. Le Moal</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author><author><name sortKey="Herman, J P" sort="Herman, J P" uniqKey="Herman J" first="J. P." last="Herman">J. P. Herman</name><affiliation><mods:affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1990">1990</date><biblScope unit="volume">526</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="195">195</biblScope><biblScope unit="page" to="202">202</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">4EFCEB24B6BC20CF15B09933429C849E063885A9</idno><idno type="DOI">10.1016/0006-8993(90)91221-2</idno><idno type="PII">0006-8993(90)91221-2</idno><idno type="ArticleID">90912212</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6-Hydroxydopamine</term><term>Dopamine</term><term>Dopamine D1 receptor</term><term>Dopamine D2 receptor</term><term>Neonatal lesion</term><term>Receptor hypersensitivity</term><term>Striatum</term><term>Turning behavior</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>D.N. Abrous</name><affiliations><json:string>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</json:string></affiliations></json:item><json:item><name>J.M. Rivet</name><affiliations><json:string>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</json:string></affiliations></json:item><json:item><name>M. Le Moal</name><affiliations><json:string>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</json:string></affiliations></json:item><json:item><name>J.P. Herman</name><affiliations><json:string>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dopamine D1 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine D2 receptor</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>6-Hydroxydopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neonatal lesion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Receptor hypersensitivity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Turning behavior</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Striatum</value></json:item></subject><articleId><json:string>90912212</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Short communication</json:string></originalGenre><abstract>Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</abstract><qualityIndicators><score>7.417</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 828 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>1466</abstractCharCount><pdfWordCount>4969</pdfWordCount><pdfCharCount>30330</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>204</abstractWordCount></qualityIndicators><title>Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title><pii><json:string>0006-8993(90)91221-2</json:string></pii><refBibs><json:item><author><json:item><name>N. Abrous</name></json:item><json:item><name>J. 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(Biomedical Division)</p></availability><date>1990</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title><author xml:id="author-1"><persName><forename type="first">D.N.</forename><surname>Abrous</surname></persName><affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation></author><author xml:id="author-2"><persName><forename type="first">J.M.</forename><surname>Rivet</surname></persName><affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation></author><author xml:id="author-3"><persName><forename type="first">M.</forename><surname>Le Moal</surname></persName><affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation></author><author xml:id="author-4"><persName><forename type="first">J.P.</forename><surname>Herman</surname></persName><note type="correspondence"><p>Correspondence: J.P. Herman, Inserm U-259-Universite´de Bordeaux II, Domaine de Carreire, rue Camille Saint-Sae¨ns, 33077 Bordeaux Cedex, France.</p></note><affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation></author></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X0710-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1990"></date><biblScope unit="volume">526</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="195">195</biblScope><biblScope unit="page" to="202">202</biblScope></imprint></monogr><idno type="istex">4EFCEB24B6BC20CF15B09933429C849E063885A9</idno><idno type="DOI">10.1016/0006-8993(90)91221-2</idno><idno type="PII">0006-8993(90)91221-2</idno><idno type="ArticleID">90912212</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1990</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dopamine D1 receptor</term></item><item><term>Dopamine D2 receptor</term></item><item><term>Dopamine</term></item><item><term>6-Hydroxydopamine</term></item><item><term>Neonatal lesion</term></item><item><term>Receptor hypersensitivity</term></item><item><term>Turning behavior</term></item><item><term>Striatum</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1990">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/4EFCEB24B6BC20CF15B09933429C849E063885A9/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="sco"><item-info><jid>BRES</jid><aid>90912212</aid><ce:pii>0006-8993(90)91221-2</ce:pii><ce:doi>10.1016/0006-8993(90)91221-2</ce:doi><ce:copyright type="unknown" year="1990">Elsevier Science Publishers B.V. (Biomedical Division)</ce:copyright></item-info><head><ce:title>Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</ce:title><ce:author-group><ce:author><ce:given-name>D.N.</ce:given-name><ce:surname>Abrous</ce:surname></ce:author><ce:author><ce:given-name>J.M.</ce:given-name><ce:surname>Rivet</ce:surname></ce:author><ce:author><ce:given-name>M.</ce:given-name><ce:surname>Le Moal</ce:surname></ce:author><ce:author><ce:given-name>J.P.</ce:given-name><ce:surname>Herman</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text><ce:italic>Correspondence:</ce:italic> J.P. Herman, Inserm U-259-Universite´de Bordeaux II, Domaine de Carreire, rue Camille Saint-Sae¨ns, 33077 Bordeaux Cedex, France.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="27" month="2" year="1990"></ce:date-accepted><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D<ce:inf loc="post">1</ce:inf> receptor blocker SCH-23390 (0.1 mg/kg) and the specific D<ce:inf loc="post">2</ce:inf> receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D<ce:inf loc="post">1</ce:inf> and D<ce:inf loc="post">2</ce:inf> dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</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>Dopamine D<ce:inf loc="post">1</ce:inf> receptor</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine D<ce:inf loc="post">2</ce:inf> receptor</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>6-Hydroxydopamine</ce:text></ce:keyword><ce:keyword><ce:text>Neonatal lesion</ce:text></ce:keyword><ce:keyword><ce:text>Receptor hypersensitivity</ce:text></ce:keyword><ce:keyword><ce:text>Turning behavior</ce:text></ce:keyword><ce:keyword><ce:text>Striatum</ce:text></ce:keyword></ce:keywords></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>Reference</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>1</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Abrous</ce:surname><ce:given-name>N.</ce:given-name></sb:author><sb:author><ce:surname>Guy</ce:surname><ce:given-name>J.</ce:given-name></sb:author><sb:author><ce:surname>Vigny</ce:surname><ce:given-name>A.</ce:given-name></sb:author><sb:author><ce:surname>Calas</ce:surname><ce:given-name>A.</ce:given-name></sb:author><sb:author><ce:surname>Le Moal</ce:surname><ce:given-name>M.</ce:given-name></sb:author><sb:author><ce:surname>Herman</ce:surname><ce:given-name>J.P.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Development of intracerebral dopaminergic grafts: a combined immunohistochemical and autoradiographic study of its time course and environmental influences</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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Herman, Inserm U-259-Universite´de Bordeaux II, Domaine de Carreire, rue Camille Saint-Sae¨ns, 33077 Bordeaux Cedex, France.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="Short communication"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1990</dateIssued><copyrightDate encoding="w3cdtf">1990</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">Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</abstract><subject lang="en"><genre>Keywords</genre><topic>Dopamine D1 receptor</topic><topic>Dopamine D2 receptor</topic><topic>Dopamine</topic><topic>6-Hydroxydopamine</topic><topic>Neonatal lesion</topic><topic>Receptor hypersensitivity</topic><topic>Turning behavior</topic><topic>Striatum</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19900903</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0710-X</identifier><part><date>19900903</date><detail type="volume"><number>526</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>181</start><end>362</end></extent><extent unit="pages"><start>195</start><end>202</end></extent></part></relatedItem><identifier type="istex">4EFCEB24B6BC20CF15B09933429C849E063885A9</identifier><identifier type="DOI">10.1016/0006-8993(90)91221-2</identifier><identifier type="PII">0006-8993(90)91221-2</identifier><identifier type="ArticleID">90912212</identifier><accessCondition type="use and reproduction" contentType="copyright">©1990 Elsevier Science Publishers B.V. 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