Sodium-dependent glutamate binding in senile dementia
Identifieur interne : 002C18 ( Main/Corpus ); précédent : 002C17; suivant : 002C19Sodium-dependent glutamate binding in senile dementia
Auteurs : Edith G. Mcgeer ; Edith A. Singh ; Patrick L. McgeerSource :
- Neurobiology of Aging [ 0197-4580 ] ; 1986.
Abstract
Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (Ka) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.
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DOI: 10.1016/0197-4580(87)90005-4
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Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7726C4F89B4F0518BA0435BEC68943C20573ACDC</idno><date when="1987" year="1987">1987</date><idno type="doi">10.1016/0197-4580(87)90005-4</idno><idno type="url">https://api.istex.fr/document/7726C4F89B4F0518BA0435BEC68943C20573ACDC/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002C18</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Sodium-dependent glutamate binding in senile dementia</title><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</mods:affiliation></affiliation></author><author><name sortKey="Singh, Edith A" sort="Singh, Edith A" uniqKey="Singh E" first="Edith A." last="Singh">Edith A. Singh</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neurobiology of Aging</title><title level="j" type="abbrev">NBA</title><idno type="ISSN">0197-4580</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1986">1986</date><biblScope unit="volume">8</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="219">219</biblScope><biblScope unit="page" to="223">223</biblScope></imprint><idno type="ISSN">0197-4580</idno></series><idno type="istex">7726C4F89B4F0518BA0435BEC68943C20573ACDC</idno><idno type="DOI">10.1016/0197-4580(87)90005-4</idno><idno type="PII">0197-4580(87)90005-4</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0197-4580</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (Ka) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Edith G. McGeer</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</json:string></affiliations></json:item><json:item><name>Edith A. Singh</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</json:string></affiliations></json:item><json:item><name>Patrick L. McGeer</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Senile dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Choline</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Acetyltransferase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Sodium-dependent</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glutamate binding</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glutamate neurons</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Postmortem delay</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (Ka) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. 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Binding affinities (Ka) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Senile dementia</term></item><item><term>Choline</term></item><item><term>Acetyltransferase</term></item><item><term>Sodium-dependent</term></item><item><term>Glutamate binding</term></item><item><term>Glutamate neurons</term></item><item><term>Postmortem delay</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1986-12-15">Received</change><change when="1986">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>NBA</jid><aid>87900054</aid><ce:pii>0197-4580(87)90005-4</ce:pii><ce:doi>10.1016/0197-4580(87)90005-4</ce:doi><ce:copyright type="unknown" year="1987"></ce:copyright></item-info><head><ce:title>Sodium-dependent glutamate binding in senile dementia</ce:title><ce:author-group><ce:author><ce:given-name>Edith G.</ce:given-name><ce:surname>McGeer</ce:surname></ce:author><ce:author><ce:given-name>Edith A.</ce:given-name><ce:surname>Singh</ce:surname></ce:author><ce:author><ce:given-name>Patrick L.</ce:given-name><ce:surname>McGeer</ce:surname></ce:author><ce:affiliation><ce:textfn>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="15" month="12" year="1986"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (K<ce:inf>a</ce:inf>) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Senile dementia</ce:text></ce:keyword><ce:keyword><ce:text>Choline</ce:text></ce:keyword><ce:keyword><ce:text>Acetyltransferase</ce:text></ce:keyword><ce:keyword><ce:text>Sodium-dependent</ce:text></ce:keyword><ce:keyword><ce:text>Glutamate binding</ce:text></ce:keyword><ce:keyword><ce:text>Glutamate neurons</ce:text></ce:keyword><ce:keyword><ce:text>Postmortem delay</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Sodium-dependent glutamate binding in senile dementia</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Sodium-dependent glutamate binding in senile dementia</title></titleInfo><name type="personal"><namePart type="given">Edith G.</namePart><namePart type="family">McGeer</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edith A.</namePart><namePart type="family">Singh</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrick L.</namePart><namePart type="family">McGeer</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada, V6T 1W5</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">1986</dateIssued><dateCaptured encoding="w3cdtf">1986-12-15</dateCaptured><copyrightDate encoding="w3cdtf">1987</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">Sodium-dependent glutamate binding was studied as a possible index of the integrity of glutamate/aspartate (Glu/Asp) nerve endings in seven cortical areas from postmortem brains of 15 persons with senile dementia of the Alzheimer type (SD), 10 controls matched for age, sex and postmortem delay (PMD), and single cases of Down's syndrome and Parkinson-dementia. Binding affinities (Ka) were quite variable from brain to brain but showed no relation to sex, age, PMD or disease. Specific binding site densities did not vary with age or sex but showed overall a significant negative correlation with PMD, a significant decrease in SD, and a significant correlation in the SD—but not the control—samples with choline acetyltransferase (ChAT) activities. The binding data on individual brain regions, however, showed no significant difference between SD cases and controls despite highly significant differences in the ChAT activities. The overall results support but do not confirm a defect in cortical Glu/Asp systems in SD. Reported and obtained data on lesioned rats are summarized to suggest that sodium-dependent glutamate binding may be an ineffective index of Glu/Asp nerve endings.</abstract><subject><genre>Keywords</genre><topic>Senile dementia</topic><topic>Choline</topic><topic>Acetyltransferase</topic><topic>Sodium-dependent</topic><topic>Glutamate binding</topic><topic>Glutamate neurons</topic><topic>Postmortem delay</topic></subject><relatedItem type="host"><titleInfo><title>Neurobiology of Aging</title></titleInfo><titleInfo type="abbreviated"><title>NBA</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">198705</dateIssued></originInfo><identifier type="ISSN">0197-4580</identifier><identifier type="PII">S0197-4580(00)X0063-2</identifier><part><date>198705</date><detail type="volume"><number>8</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue pages"><start>193</start><end>290</end></extent><extent unit="pages"><start>219</start><end>223</end></extent></part></relatedItem><identifier type="istex">7726C4F89B4F0518BA0435BEC68943C20573ACDC</identifier><identifier type="DOI">10.1016/0197-4580(87)90005-4</identifier><identifier type="PII">0197-4580(87)90005-4</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/7726C4F89B4F0518BA0435BEC68943C20573ACDC/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">GERIATRICS & GERONTOLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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