Involvement of GABAA receptors in myoclonus
Identifieur interne : 001D96 ( Istex/Corpus ); précédent : 001D95; suivant : 001D97Involvement of GABAA receptors in myoclonus
Auteurs : Rae R. Matsumoto ; Daniel D. Truong ; Kevin D. Nguyen ; A. Terri Dang ; Tin T. Hoang ; Phi Q. Vo ; Paola SandroniSource :
- Movement Disorders [ 0885-3185 ] ; 2000-09.
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- KwdEn :
Abstract
Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABAA antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.
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DOI: 10.1002/mds.870150709
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ISTEX:0850B22E396E532D4D75C2F3D63FC0957520EB35Le document en format XML
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Vo</name><affiliation><mods:affiliation>University of California Irvine, Department of Neurology, Irvine, California</mods:affiliation></affiliation></author><author><name sortKey="Sandroni, Paola" sort="Sandroni, Paola" uniqKey="Sandroni P" first="Paola" last="Sandroni">Paola Sandroni</name><affiliation><mods:affiliation>University of California Irvine, Department of Neurology, Irvine, California</mods:affiliation></affiliation><affiliation><mods:affiliation>Mayo Clinic, Department of Neurology, Rochester, Minnesota, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABAA antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Rae R. Matsumoto PhD</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string><json:string>University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology, Oklahoma City, Oklahoma</json:string></affiliations></json:item><json:item><name>Daniel D. Truong MD</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string><json:string>Long Beach Memorial Medical Center, Long Beach, California</json:string></affiliations></json:item><json:item><name>Kevin D. Nguyen MD</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string></affiliations></json:item><json:item><name>A. Terri Dang BS</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string></affiliations></json:item><json:item><name>Tin T. Hoang BS</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string></affiliations></json:item><json:item><name>Phi Q. Vo MD</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string></affiliations></json:item><json:item><name>Paola Sandroni MD</name><affiliations><json:string>University of California Irvine, Department of Neurology, Irvine, California</json:string><json:string>Mayo Clinic, Department of Neurology, Rochester, Minnesota, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Myoclonus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GABA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Nucleus reticularis thalami</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Caudate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cortex</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABAA antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.</abstract><qualityIndicators><score>5.499</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792.24 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractCharCount>1357</abstractCharCount><pdfWordCount>3219</pdfWordCount><pdfCharCount>20650</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>Involvement of GABAA receptors in myoclonus</title><genre><json:string>Serial article</json:string></genre><host><volume>15</volume><pages><total>6</total><last>52</last><first>47</first></pages><issn><json:string>0885-3185</json:string></issn><issue>S1</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2000</publicationDate><copyrightDate>2000</copyrightDate><doi><json:string>10.1002/mds.870150709</json:string></doi><id>0850B22E396E532D4D75C2F3D63FC0957520EB35</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/0850B22E396E532D4D75C2F3D63FC0957520EB35/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/0850B22E396E532D4D75C2F3D63FC0957520EB35/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0850B22E396E532D4D75C2F3D63FC0957520EB35/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Involvement of GABAA receptors in myoclonus</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2000</date></publicationStmt><notesStmt><note>NIH - No. K08NSO1681;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Involvement of GABAA receptors in myoclonus</title><author><persName><forename type="first">Rae R.</forename><surname>Matsumoto</surname><roleName type="degree">PhD</roleName></persName><note type="correspondence"><p>Correspondence: University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology, PO Box 26901, CPB 229, Oklahoma City, OK 73190, U.S.A.</p></note><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><affiliation>University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology, Oklahoma City, Oklahoma</affiliation></author><author><persName><forename type="first">Daniel D.</forename><surname>Truong</surname><roleName type="degree">MD</roleName></persName><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><affiliation>Long Beach Memorial Medical Center, Long Beach, California</affiliation></author><author><persName><forename type="first">Kevin D.</forename><surname>Nguyen</surname><roleName type="degree">MD</roleName></persName><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation></author><author><persName><forename type="first">A. 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It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABAA antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Myoclonus</term></item><item><term>GABA</term></item><item><term>Nucleus reticularis thalami</term></item><item><term>Caudate</term></item><item><term>Cortex</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0850B22E396E532D4D75C2F3D63FC0957520EB35/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABA<sub>A</sub> antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABA<sub>A</sub>, but not GABA<sub>B</sub>, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABA<sub>A</sub> antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABA<sub>A</sub> receptors at any one of a number of levels in the neural axis can produce myoclonus.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Involvement of GABAA receptors in myoclonus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>INVOLVEMENT OF GABAA, RECEPTORS IN MYOCLONUS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Involvement of GABA</title></titleInfo><name type="personal"><namePart type="given">Rae R.</namePart><namePart type="family">Matsumoto</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><affiliation>University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology, Oklahoma City, Oklahoma</affiliation><description>Correspondence: University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology, PO Box 26901, CPB 229, Oklahoma City, OK 73190, U.S.A.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel D.</namePart><namePart type="family">Truong</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><affiliation>Long Beach Memorial Medical Center, Long Beach, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kevin D.</namePart><namePart type="family">Nguyen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. Terri</namePart><namePart type="family">Dang</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tin T.</namePart><namePart type="family">Hoang</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Phi Q.</namePart><namePart type="family">Vo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Sandroni</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of California Irvine, Department of Neurology, Irvine, California</affiliation><affiliation>Mayo Clinic, Department of Neurology, Rochester, Minnesota, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2000-09</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent></physicalDescription><abstract lang="en">Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABAA antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.</abstract><note type="funding">NIH - No. K08NSO1681; </note><subject lang="en"><genre>Keywords</genre><topic>Myoclonus</topic><topic>GABA</topic><topic>Nucleus reticularis thalami</topic><topic>Caudate</topic><topic>Cortex</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>S1</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>S1</number></detail><extent unit="pages"><start>47</start><end>52</end><total>6</total></extent></part></relatedItem><identifier type="istex">0850B22E396E532D4D75C2F3D63FC0957520EB35</identifier><identifier type="DOI">10.1002/mds.870150709</identifier><identifier type="ArticleID">MDS870150709</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2000 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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