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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<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>
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<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.</abstract>
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<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>
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<author xml:id="author-2"><persName><forename type="first">Yves</forename>
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<author xml:id="author-3"><persName><forename type="first">Etienne C.</forename>
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<note type="correspondence"><p>Corresponding author. Fax: (33) (1) 44 24 36 58.</p>
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<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>
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<item><term>Calcium binding protein</term>
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<item><term>Tyrosine hydroxylase</term>
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<item><term>Mesencephalon</term>
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<item><term>Parkinson's disease</term>
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<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>
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<mods version="3.6"><titleInfo lang="en"><title>Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</title>
</titleInfo>
<titleInfo type="alternative" lang="en" contentType="CDATA"><title>Does the calcium binding protein calretinin protect dopaminergic neurons against degeneration in Parkinson's disease?</title>
</titleInfo>
<name type="personal"><namePart type="given">Annick</namePart>
<namePart type="family">Mouatt-Prigent</namePart>
<affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Yves</namePart>
<namePart type="family">Agid</namePart>
<affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Etienne C.</namePart>
<namePart type="family">Hirsch</namePart>
<affiliation>INSERM U289, Hoˆpital de la Salpêtrière, 47 boulevard de l'Hoˆpital, 75013 Paris ,France</affiliation>
<description>Corresponding author. Fax: (33) (1) 44 24 36 58.</description>
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</role>
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<copyrightDate encoding="w3cdtf">1994</copyrightDate>
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<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>
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<genre type="journal">journal</genre>
<originInfo><dateIssued encoding="w3cdtf">19941230</dateIssued>
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<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>
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<detail type="issue"><number>1–2</number>
<caption>no.</caption>
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<extent unit="issue pages"><start>1</start>
<end>278</end>
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<extent unit="pages"><start>62</start>
<end>70</end>
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<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. All rights reserved</accessCondition>
<recordInfo><recordContentSource>ELSEVIER</recordContentSource>
<recordOrigin>Elsevier Science B.V. All rights reserved, ©1994</recordOrigin>
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