Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types
Identifieur interne : 000507 ( Main/Corpus ); précédent : 000506; suivant : 000508Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types
Auteurs : K. Perry ; J. Smith ; A. Court ; H. PerrySource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1990-09-01.
Abstract
Summary: Cholinergic nicotinic and muscarinic receptor binding were measured in post mortem human brain tissue, using low (nM) concentrations of (3H)-nicotine to detect predominately the high affinity nicotinic site and (3H)-N-methylscopolamine in the presence and absence of 3×10−4 M carbachol to measure both the low and high affinity agonist subtypes of the muscarinic receptor group. Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (3H)-nicotine binding displaced by a range of carbachol concentrations (10−9–10−3 M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. This observation raised the question of whether the presence of neurofibrilalry tangles (evident in the latter but not former 2 disorders) is incompatible with denervation-induced muscarinic supersensitivity in cholinoceptive neurons which include cortical pyramids generally affeced by tangle formation.
Url:
DOI: 10.1007/BF02257646
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Court</name><affiliation><mods:affiliation>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author><author><name sortKey="Perry, H" sort="Perry, H" uniqKey="Perry H" first="H." last="Perry">H. Perry</name><affiliation><mods:affiliation>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:527291CB4A67B00CE35C2323B00A407F77709DCC</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1007/BF02257646</idno><idno type="url">https://api.istex.fr/document/527291CB4A67B00CE35C2323B00A407F77709DCC/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000507</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types</title><author><name sortKey="Perry, K" sort="Perry, K" uniqKey="Perry K" first="K." last="Perry">K. Perry</name><affiliation><mods:affiliation>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author><author><name sortKey="Smith, J" sort="Smith, J" uniqKey="Smith J" first="J." last="Smith">J. Smith</name><affiliation><mods:affiliation>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author><author><name sortKey="Court, A" sort="Court, A" uniqKey="Court A" first="A." last="Court">A. Court</name><affiliation><mods:affiliation>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author><author><name sortKey="Perry, H" sort="Perry, H" uniqKey="Perry H" first="H." last="Perry">H. Perry</name><affiliation><mods:affiliation>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="ISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1990-09-01">1990-09-01</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="149">149</biblScope><biblScope unit="page" to="158">158</biblScope></imprint><idno type="ISSN">0936-3076</idno></series><idno type="istex">527291CB4A67B00CE35C2323B00A407F77709DCC</idno><idno type="DOI">10.1007/BF02257646</idno><idno type="ArticleID">Art1</idno><idno type="ArticleID">BF02257646</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0936-3076</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Cholinergic nicotinic and muscarinic receptor binding were measured in post mortem human brain tissue, using low (nM) concentrations of (3H)-nicotine to detect predominately the high affinity nicotinic site and (3H)-N-methylscopolamine in the presence and absence of 3×10−4 M carbachol to measure both the low and high affinity agonist subtypes of the muscarinic receptor group. Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (3H)-nicotine binding displaced by a range of carbachol concentrations (10−9–10−3 M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. This observation raised the question of whether the presence of neurofibrilalry tangles (evident in the latter but not former 2 disorders) is incompatible with denervation-induced muscarinic supersensitivity in cholinoceptive neurons which include cortical pyramids generally affeced by tangle formation.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Dr. E. K. Perry</name><affiliations><json:string>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</json:string></affiliations></json:item><json:item><name>C. J. Smith</name><affiliations><json:string>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</json:string></affiliations></json:item><json:item><name>J. A. Court</name><affiliations><json:string>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</json:string></affiliations></json:item><json:item><name>R. H. Perry</name><affiliations><json:string>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</json:string></affiliations></json:item></author><articleId><json:string>Art1</json:string><json:string>BF02257646</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Cholinergic nicotinic and muscarinic receptor binding were measured in post mortem human brain tissue, using low (nM) concentrations of (3H)-nicotine to detect predominately the high affinity nicotinic site and (3H)-N-methylscopolamine in the presence and absence of 3×10−4 M carbachol to measure both the low and high affinity agonist subtypes of the muscarinic receptor group. Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (3H)-nicotine binding displaced by a range of carbachol concentrations (10−9–10−3 M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. 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Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (3H)-nicotine binding displaced by a range of carbachol concentrations (10−9–10−3 M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. This observation raised the question of whether the presence of neurofibrilalry tangles (evident in the latter but not former 2 disorders) is incompatible with denervation-induced muscarinic supersensitivity in cholinoceptive neurons which include cortical pyramids generally affeced by tangle formation.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1990-02-05">Created</change><change when="1990-09-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/527291CB4A67B00CE35C2323B00A407F77709DCC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>722</JournalID><JournalPrintISSN>0936-3076</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</JournalTitle><JournalAbbreviatedTitle>J Neural Transm Gen Sect</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd><IssueArticleCount>10</IssueArticleCount><IssueHistory><CoverDate><DateString>1990</DateString><Year>1990</Year><Month>9</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF02257646</ArticleID><ArticleDOI>10.1007/BF02257646</ArticleDOI><ArticleSequenceNumber>1</ArticleSequenceNumber><ArticleTitle Language="En">Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types</ArticleTitle><ArticleFirstPage>149</ArticleFirstPage><ArticleLastPage>158</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>11</Month><Day>5</Day></RegistrationDate><Received><Year>1990</Year><Month>2</Month><Day>5</Day></Received><Accepted><Year>1990</Year><Month>5</Month><Day>5</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>722</JournalID><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><Prefix>Dr.</Prefix><GivenName>E.</GivenName><GivenName>K.</GivenName><FamilyName>Perry</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2" PresentAffiliationID="Aff3"><AuthorName DisplayOrder="Western"><GivenName>C.</GivenName><GivenName>J.</GivenName><FamilyName>Smith</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>J.</GivenName><GivenName>A.</GivenName><FamilyName>Court</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><GivenName>H.</GivenName><FamilyName>Perry</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>MRC Neurochemical Pathology Unit</OrgDivision><OrgName>Newcastle General Hospital</OrgName><OrgAddress><Street>Westgate Road</Street><Postcode>NE46BE</Postcode><City>Newcastle upon Tyne</City><Country>UK</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Neuropathology</OrgDivision><OrgName>Newcastle General Hospital</OrgName><OrgAddress><Street>Westgate Road</Street><Postcode>NE46BE</Postcode><City>Newcastle upon Tyne</City><Country>UK</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>INSERM U298</OrgDivision><OrgName>Centre Hospitalier, Regional Universitaire</OrgName><OrgAddress><Postcode>F-49033</Postcode><City>Angers Cedex</City><Country>France</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Cholinergic nicotinic and muscarinic receptor binding were measured in post mortem human brain tissue, using low (nM) concentrations of (<Superscript>3</Superscript>H)-nicotine to detect predominately the high affinity nicotinic site and (<Superscript>3</Superscript>H)-N-methylscopolamine in the presence and absence of 3×10<Superscript>−4</Superscript> M carbachol to measure both the low and high affinity agonist subtypes of the muscarinic receptor group. Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (<Superscript>3</Superscript>H)-nicotine binding displaced by a range of carbachol concentrations (10<Superscript>−9</Superscript>–10<Superscript>−3</Superscript> M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. This observation raised the question of whether the presence of neurofibrilalry tangles (evident in the latter but not former 2 disorders) is incompatible with denervation-induced muscarinic supersensitivity in cholinoceptive neurons which include cortical pyramids generally affeced by tangle formation.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Nicotinic receptor</Keyword><Keyword>muscarinic receptor</Keyword><Keyword>Alzheimer's disease</Keyword><Keyword>Parkinson's disease</Keyword><Keyword>senile dementia of Lewy body type</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cholinergic nicotinic and muscarinic receptors in dementia of Alzheimer, Parkinson and Lewy body types</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="given">E.</namePart><namePart type="given">K.</namePart><namePart type="family">Perry</namePart><affiliation>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="given">J.</namePart><namePart type="family">Smith</namePart><affiliation>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="given">A.</namePart><namePart type="family">Court</namePart><affiliation>MRC Neurochemical Pathology Unit, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="given">H.</namePart><namePart type="family">Perry</namePart><affiliation>Department of Neuropathology, Newcastle General Hospital, Westgate Road, NE46BE, Newcastle upon Tyne, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1990-02-05</dateCreated><dateIssued encoding="w3cdtf">1990-09-01</dateIssued><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Cholinergic nicotinic and muscarinic receptor binding were measured in post mortem human brain tissue, using low (nM) concentrations of (3H)-nicotine to detect predominately the high affinity nicotinic site and (3H)-N-methylscopolamine in the presence and absence of 3×10−4 M carbachol to measure both the low and high affinity agonist subtypes of the muscarinic receptor group. Consistent with most previous reports, the nicotinic but not muscarinic binding was reduced in the different forms of dementia associated with cortical cholinergic deficits, including Alzheimer's and Parkinson's disease, senile dementia of Lewy body type (SDLT) and Down's syndrome (over 50 years). Analysis of (3H)-nicotine binding displaced by a range of carbachol concentrations (10−9–10−3 M) indicated 2 binding sites for nicotine and that the high affinity rather than low affinity site was reduced in Alzheimer's disease. In all 3 cortical areas investigated (temporal, parietal and occipital) there were increases in the low affinity muscarinic site in Parkinson's disease and SDLT but not Alzheimer's disease or middle-aged Down's syndrome. This observation raised the question of whether the presence of neurofibrilalry tangles (evident in the latter but not former 2 disorders) is incompatible with denervation-induced muscarinic supersensitivity in cholinoceptive neurons which include cortical pyramids generally affeced by tangle formation.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title></titleInfo><titleInfo type="abbreviated"><title>J Neural Transm Gen Sect</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1990-09-01</dateIssued><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Psychiatry</topic><topic>Neurology</topic></subject><identifier type="ISSN">0936-3076</identifier><identifier type="eISSN">1435-1463</identifier><identifier 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