Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?
Identifieur interne : 001A75 ( Istex/Corpus ); précédent : 001A74; suivant : 001A76Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?
Auteurs : Annick Mouatt-Prigent ; Yves Agid ; Etienne C. HirschSource :
- Brain Research [ 0006-8993 ] ; 1994.
English descriptors
Abstract
Abstract: Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR+ dopaminergic neurons was observed, suggesting a neuroprotective role in some dopaminergic cell groups only.
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DOI: 10.1016/0006-8993(94)90511-8
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Hirsch</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:28498A4DCDF24F2114BDDFAB7D43925455B0BFA8</idno><date when="1994" year="1994">1994</date><idno type="doi">10.1016/0006-8993(94)90511-8</idno><idno type="url">https://api.istex.fr/document/28498A4DCDF24F2114BDDFAB7D43925455B0BFA8/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001A75</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001A75</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</title><author><name sortKey="Mouatt Prigent, Annick" sort="Mouatt Prigent, Annick" uniqKey="Mouatt Prigent A" first="Annick" last="Mouatt-Prigent">Annick Mouatt-Prigent</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><affiliation><mods:affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,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="1994">1994</date><biblScope unit="volume">668</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="62">62</biblScope><biblScope unit="page" to="70">70</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">28498A4DCDF24F2114BDDFAB7D43925455B0BFA8</idno><idno type="DOI">10.1016/0006-8993(94)90511-8</idno><idno type="PII">0006-8993(94)90511-8</idno><idno type="ArticleID">94905118</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Calcium binding protein</term><term>Human</term><term>Mesencephalon</term><term>Parkinson's disease</term><term>Tyrosine hydroxylase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR+ dopaminergic neurons was observed, suggesting a neuroprotective role in some dopaminergic cell groups only.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Annick Mouatt-Prigent</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</json:string></affiliations></json:item><json:item><name>Yves Agid</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</json:string></affiliations></json:item><json:item><name>Etienne C. Hirsch</name><affiliations><json:string>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Calcium binding protein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Tyrosine hydroxylase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Mesencephalon</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Human</value></json:item></subject><articleId><json:string>94905118</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Short communication</json:string></originalGenre><abstract>Abstract: Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. 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USA</title></serie><host><volume>668</volume><pii><json:string>S0006-8993(00)X1567-3</json:string></pii><pages><last>70</last><first>62</first></pages><issn><json:string>0006-8993</json:string></issn><issue>1–2</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Brain Research</title><publicationDate>1994</publicationDate></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1016/0006-8993(94)90511-8</json:string></doi><id>28498A4DCDF24F2114BDDFAB7D43925455B0BFA8</id><score>0.15456265</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/28498A4DCDF24F2114BDDFAB7D43925455B0BFA8/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/28498A4DCDF24F2114BDDFAB7D43925455B0BFA8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/28498A4DCDF24F2114BDDFAB7D43925455B0BFA8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1994 Elsevier Science B.V. All rights reserved</p></availability><date>1994</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</title><author xml:id="author-1"><persName><forename type="first">Annick</forename><surname>Mouatt-Prigent</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Etienne C.</forename><surname>Hirsch</surname></persName><note type="correspondence"><p>Corresponding author. Fax: (33) (1) 44 24 36 58.</p></note><affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,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)X1567-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994"></date><biblScope unit="volume">668</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="62">62</biblScope><biblScope unit="page" to="70">70</biblScope></imprint></monogr><idno type="istex">28498A4DCDF24F2114BDDFAB7D43925455B0BFA8</idno><idno type="DOI">10.1016/0006-8993(94)90511-8</idno><idno type="PII">0006-8993(94)90511-8</idno><idno type="ArticleID">94905118</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR+ dopaminergic neurons was observed, suggesting a neuroprotective role in some dopaminergic cell groups only.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Calcium binding protein</term></item><item><term>Tyrosine hydroxylase</term></item><item><term>Mesencephalon</term></item><item><term>Parkinson's disease</term></item><item><term>Human</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/28498A4DCDF24F2114BDDFAB7D43925455B0BFA8/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>94905118</aid><ce:pii>0006-8993(94)90511-8</ce:pii><ce:doi>10.1016/0006-8993(94)90511-8</ce:doi><ce:copyright type="unknown" year="1994">Elsevier Science B.V. All rights reserved</ce:copyright></item-info><head><ce:title>Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</ce:title><ce:author-group><ce:author><ce:given-name>Annick</ce:given-name><ce:surname>Mouatt-Prigent</ce:surname></ce:author><ce:author><ce:given-name>Yves</ce:given-name><ce:surname>Agid</ce:surname></ce:author><ce:author><ce:given-name>Etienne C.</ce:given-name><ce:surname>Hirsch</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text>Corresponding author. Fax: (33) (1) 44 24 36 58.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="27" month="9" year="1994"></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">Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR<ce:sup loc="post">+</ce:sup>) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR<ce:sup loc="post">+</ce:sup> neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR<ce:sup loc="post">+</ce:sup> neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR<ce:sup loc="post">+</ce:sup> dopaminergic neurons was observed, suggesting a neuroprotective role in some dopaminergic cell groups only.</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>Calcium binding protein</ce:text></ce:keyword><ce:keyword><ce:text>Tyrosine hydroxylase</ce:text></ce:keyword><ce:keyword><ce:text>Mesencephalon</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Human</ce:text></ce:keyword></ce:keywords></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>References</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>Baimbridge</ce:surname><ce:given-name>K.G.</ce:given-name></sb:author><sb:author><ce:surname>Celio</ce:surname><ce:given-name>M.R.</ce:given-name></sb:author><sb:author><ce:surname>Rogers</ce:surname><ce:given-name>J.H.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Calcium-binding proteins in the nervous system</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Trends Neurosci.</sb:maintitle></sb:title><sb:volume-nr>15</sb:volume-nr></sb:series><sb:date>1992</sb:date></sb:issue><sb:pages><sb:first-page>303</sb:first-page><sb:last-page>308</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 langtype="en"><sb:authors><sb:author><ce:surname>Damier</ce:surname><ce:given-name>P.</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>Zhang</ce:surname><ce:given-name>P.</ce:given-name></sb:author><sb:author><ce:surname>Agid</ce:surname><ce:given-name>Y.</ce:given-name></sb:author><sb:author><ce:surname>Javoy-Agid</ce:surname><ce:given-name>F.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Glutathione peroxidase, glial cells and Parkinson's disease</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Neuroscience</sb:maintitle></sb:title><sb:volume-nr>52</sb:volume-nr></sb:series><sb:date>1993</sb:date></sb:issue><sb:pages><sb:first-page>1</sb:first-page><sb:last-page>6</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib3"><ce:label>[3]</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Dexter</ce:surname><ce:given-name>D.T.</ce:given-name></sb:author><sb:author><ce:surname>Wells</ce:surname><ce:given-name>F.R.</ce:given-name></sb:author><sb:author><ce:surname>Lees</ce:surname><ce:given-name>A.J.</ce:given-name></sb:author><sb:author><ce:surname>Agid</ce:surname><ce:given-name>F.</ce:given-name></sb:author><sb:author><ce:surname>Agid</ce:surname><ce:given-name>Y.</ce:given-name></sb:author><sb:author><ce:surname>Jenner</ce:surname><ce:given-name>P.</ce:given-name></sb:author><sb:author><ce:surname>Marsden</ce:surname><ce:given-name>C.D.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>Increased nigral iron content and alterations in other metal ions occuring in brain in Parkinson's disease</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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Fax: (33) (1) 44 24 36 58.</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">1994</dateIssued><copyrightDate encoding="w3cdtf">1994</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: Parkinson's disease (PD) is characterized by a heterogeneous loss of dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other dopaminergic cell groups. A rise in intracellular calcium concentrations represents one of the final events leading to nerve cell death. Calbindin D28k, a protein capable of buffering intracellular calcium concentrations is present in the dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among dopaminergic neurons: moderate co-localization was found in catecholaminergic cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR+ dopaminergic neurons was observed, suggesting a neuroprotective role in some dopaminergic cell groups only.</abstract><subject lang="en"><genre>Keywords</genre><topic>Calcium binding protein</topic><topic>Tyrosine hydroxylase</topic><topic>Mesencephalon</topic><topic>Parkinson's disease</topic><topic>Human</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">19941230</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X1567-3</identifier><part><date>19941230</date><detail type="volume"><number>668</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>278</end></extent><extent unit="pages"><start>62</start><end>70</end></extent></part></relatedItem><identifier type="istex">28498A4DCDF24F2114BDDFAB7D43925455B0BFA8</identifier><identifier type="DOI">10.1016/0006-8993(94)90511-8</identifier><identifier type="PII">0006-8993(94)90511-8</identifier><identifier type="ArticleID">94905118</identifier><accessCondition type="use and reproduction" contentType="copyright">©1994 Elsevier Science B.V. 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