Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?
Identifieur interne : 002D40 ( Main/Corpus ); précédent : 002D39; suivant : 002D41Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?
Auteurs : A. Mouatt-Prigent ; J. O. Karlsson ; Y. Agid ; E. C. HirschSource :
- Neuroscience [ 0306-4522 ] ; 1996.
English descriptors
- KwdEn :
Abstract
Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.
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DOI: 10.1016/0306-4522(96)00100-5
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</title><author><name sortKey="Mouatt Prigent, A" sort="Mouatt Prigent, A" uniqKey="Mouatt Prigent A" first="A." last="Mouatt-Prigent">A. Mouatt-Prigent</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Karlsson, J O" sort="Karlsson, J O" uniqKey="Karlsson J" first="J. O." last="Karlsson">J. O. Karlsson</name><affiliation><mods:affiliation>Institute of Neurobiology, University of Goteborg, P.O. Box 33031, S-400 33 Göteborg, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation><mods:affiliation>To whom all correspondence should be addressed</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:C99D9559849114DDA357418018F21B272E312E49</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1016/0306-4522(96)00100-5</idno><idno type="url">https://api.istex.fr/document/C99D9559849114DDA357418018F21B272E312E49/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002D40</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</title><author><name sortKey="Mouatt Prigent, A" sort="Mouatt Prigent, A" uniqKey="Mouatt Prigent A" first="A." last="Mouatt-Prigent">A. Mouatt-Prigent</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Karlsson, J O" sort="Karlsson, J O" uniqKey="Karlsson J" first="J. O." last="Karlsson">J. O. Karlsson</name><affiliation><mods:affiliation>Institute of Neurobiology, University of Goteborg, P.O. Box 33031, S-400 33 Göteborg, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation><mods:affiliation>To whom all correspondence should be addressed</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuroscience</title><title level="j" type="abbrev">NSC</title><idno type="ISSN">0306-4522</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">73</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="979">979</biblScope><biblScope unit="page" to="987">987</biblScope></imprint><idno type="ISSN">0306-4522</idno></series><idno type="istex">C99D9559849114DDA357418018F21B272E312E49</idno><idno type="DOI">10.1016/0306-4522(96)00100-5</idno><idno type="PII">0306-4522(96)00100-5</idno><idno type="ArticleID">96001005</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PSP</term><term>SND</term><term>calcium</term><term>cell death</term><term>dopamine</term><term>parkinsonism</term><term>protease</term><term>substantia nigra</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>A. Mouatt-Prigent</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>J.O. Karlsson</name><affiliations><json:string>Institute of Neurobiology, University of Goteborg, P.O. Box 33031, S-400 33 Göteborg, Sweden</json:string></affiliations></json:item><json:item><name>Y. Agid</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>E.C. Hirsch</name><affiliations><json:string>To whom all correspondence should be addressed</json:string><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>calcium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cell death</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>protease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PSP : progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SND : striatonigral degeneration</value></json:item></subject><articleId><json:string>96001005</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</abstract><qualityIndicators><score>7.664</score><pdfVersion>1.3</pdfVersion><pdfPageSize>540 x 778 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>1682</abstractCharCount><pdfWordCount>5423</pdfWordCount><pdfCharCount>35452</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>222</abstractWordCount></qualityIndicators><title>Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</title><pii><json:string>0306-4522(96)00100-5</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>Vol. 5</volume><editor><json:item><name>M.D. Yahr</name></json:item><json:item><name>K.J. 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Box 33031, S-400 33 Göteborg, Sweden</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Agid</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</affiliation></author><author><persName><forename type="first">E.C.</forename><surname>Hirsch</surname></persName><affiliation>To whom all correspondence should be addressed</affiliation><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</affiliation></author></analytic><monogr><title level="j">Neuroscience</title><title level="j" type="abbrev">NSC</title><idno type="pISSN">0306-4522</idno><idno type="PII">S0306-4522(00)X0002-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996"></date><biblScope unit="volume">73</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="979">979</biblScope><biblScope unit="page" to="987">987</biblScope></imprint></monogr><idno type="istex">C99D9559849114DDA357418018F21B272E312E49</idno><idno type="DOI">10.1016/0306-4522(96)00100-5</idno><idno type="PII">0306-4522(96)00100-5</idno><idno type="ArticleID">96001005</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>dopamine</term></item><item><term>calcium</term></item><item><term>cell death</term></item><item><term>substantia nigra</term></item><item><term>parkinsonism</term></item><item><term>protease</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><item><term>PSP</term><term>progressive supranuclear palsy</term></item><item><term>SND</term><term>striatonigral degeneration</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-02-19">Registration</change><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></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="fla"><item-info><jid>NSC</jid><aid>96001005</aid><ce:pii>0306-4522(96)00100-5</ce:pii><ce:doi>10.1016/0306-4522(96)00100-5</ce:doi><ce:copyright type="unknown" year="1996">IBRO. All rights reserved</ce:copyright></item-info><head><ce:title>Increased m-calpain expression in the mesencephalon of patients with parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</ce:title><ce:author-group><ce:author><ce:given-name>A.</ce:given-name><ce:surname>Mouatt-Prigent</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.O.</ce:given-name><ce:surname>Karlsson</ce:surname><ce:cross-ref refid="aff2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Y.</ce:given-name><ce:surname>Agid</ce:surname><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>E.C.</ce:given-name><ce:surname>Hirsch</ce:surname><ce:cross-ref refid="cor1"><ce:sup>‡</ce:sup></ce:cross-ref><ce:cross-ref refid="aff1"><ce:sup>*</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="aff1"><ce:label>a</ce:label><ce:textfn>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</ce:textfn></ce:affiliation><ce:affiliation id="aff2"><ce:label>b</ce:label><ce:textfn>Institute of Neurobiology, University of Goteborg, P.O. Box 33031, S-400 33 Göteborg, Sweden</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>‡</ce:label><ce:text>To whom all correspondence should be addressed</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="19" month="2" year="1996"></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>Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.</ce:simple-para><ce:simple-para>These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</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</ce:text></ce:keyword><ce:keyword><ce:text>calcium</ce:text></ce:keyword><ce:keyword><ce:text>cell death</ce:text></ce:keyword><ce:keyword><ce:text>substantia nigra</ce:text></ce:keyword><ce:keyword><ce:text>parkinsonism</ce:text></ce:keyword><ce:keyword><ce:text>protease</ce:text></ce:keyword></ce:keywords><ce:keywords class="abr" xml:lang="en"><ce:keyword><ce:text>PSP</ce:text><ce:keyword><ce:text>progressive supranuclear palsy</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>SND</ce:text><ce:keyword><ce:text>striatonigral degeneration</ce:text></ce:keyword></ce:keyword></ce:keywords></head><tail><ce:bibliography><ce:section-title>Reference</ce:section-title><ce:bibliography-sec><ce:bib-reference id="bib1"><ce:label>1.</ce:label><sb:reference><sb:contribution><sb:authors><sb:author><ce:surname>Abbadie</ce:surname><ce:given-name>C.</ce:given-name></sb:author><sb:author><ce:surname>Kabrun</ce:surname><ce:given-name>N.</ce:given-name></sb:author><sb:author><ce:surname>Bouali</ce:surname><ce:given-name>F.</ce:given-name></sb:author><sb:author><ce:surname>Smardova</ce:surname><ce:given-name>J.</ce:given-name></sb:author><sb:author><ce:surname>Stehelin</ce:surname><ce:given-name>D.</ce:given-name></sb:author><sb:author><ce:surname>Vandenbunder</ce:surname><ce:given-name>B.</ce:given-name></sb:author><sb:author><ce:surname>Enrietto</ce:surname><ce:given-name>P.J.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>High levels of c-rel expression are associated with programmed cell death in the developing avian embryo and in bone marrow cells <ce:italic>in vitro</ce:italic></sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Cell</sb:maintitle></sb:title><sb:volume-nr>75</sb:volume-nr></sb:series><sb:date>1993</sb:date></sb:issue><sb:pages><sb:first-page>899</sb:first-page><sb:last-page>912</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib2"><ce:label>2.</ce:label><sb:reference><sb:contribution><sb:authors><sb:author><ce:surname>Anglade</ce:surname><ce:given-name>P.</ce:given-name></sb:author><sb:author><ce:surname>Vyas</ce:surname><ce:given-name>S.</ce:given-name></sb:author><sb:author><ce:surname>Javoy-Agid</ce:surname><ce:given-name>F.</ce:given-name></sb:author><sb:author><ce:surname>Herrero</ce:surname><ce:given-name>M.T.</ce:given-name></sb:author><sb:author><ce:surname>Michel</ce:surname><ce:given-name>P.M.</ce:given-name></sb:author><sb:author><ce:surname>Marquez</ce:surname><ce:given-name>J.</ce:given-name></sb:author><sb:author><ce:surname>Mouatt-Prigent</ce:surname><ce:given-name>A.</ce:given-name></sb:author><sb:author><ce:surname>Ruberg</ce:surname><ce:given-name>M.</ce:given-name></sb:author><sb:author><ce:surname>Hirsch</ce:surname><ce:given-name>E.C.</ce:given-name></sb:author><sb:author><ce:surname>Agid</ce:surname><ce:given-name>Y.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Apoptosic degeneration of nigral dopaminergic neurons in Parkinson's disease</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Soc. 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Box 33031, S-400 33 Göteborg, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.C.</namePart><namePart type="family">Hirsch</namePart><affiliation>To whom all correspondence should be addressed</affiliation><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 bd de 1'h^opital, 75013 Paris, France</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">1996</dateIssued><dateValid encoding="w3cdtf">1996-02-19</dateValid><copyrightDate encoding="w3cdtf">1996</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">Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures.These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>dopamine</topic><topic>calcium</topic><topic>cell death</topic><topic>substantia nigra</topic><topic>parkinsonism</topic><topic>protease</topic></subject><subject lang="en"><topic>PSP : progressive supranuclear palsy</topic><topic>SND : striatonigral degeneration</topic></subject><relatedItem type="host"><titleInfo><title>Neuroscience</title></titleInfo><titleInfo type="abbreviated"><title>NSC</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199608</dateIssued></originInfo><identifier type="ISSN">0306-4522</identifier><identifier type="PII">S0306-4522(00)X0002-4</identifier><part><detail type="volume"><number>73</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>903</start><end>1174</end></extent><extent unit="pages"><start>979</start><end>987</end></extent></part></relatedItem><identifier type="istex">C99D9559849114DDA357418018F21B272E312E49</identifier><identifier type="DOI">10.1016/0306-4522(96)00100-5</identifier><identifier type="PII">0306-4522(96)00100-5</identifier><identifier type="ArticleID">96001005</identifier><accessCondition type="use and reproduction" contentType="">© 1996IBRO. 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