Sparing of the dopaminergic neurons containing calbindin-D28k and of the dopaminergic mesocortical projections in weaver mutant mice.
Identifieur interne : 001675 ( PubMed/Corpus ); précédent : 001674; suivant : 001676Sparing of the dopaminergic neurons containing calbindin-D28k and of the dopaminergic mesocortical projections in weaver mutant mice.
Auteurs : P. Gaspar ; N. Ben Jelloun ; A. FebvretSource :
- Neuroscience [ 0306-4522 ] ; 1994.
English descriptors
- KwdEn :
- Afferent Pathways (pathology), Animals, Calbindin 1, Calbindins, Cell Nucleus (chemistry), Corpus Striatum (metabolism), Corpus Striatum (pathology), Cytoplasm (chemistry), Disease Models, Animal, Dopamine (analysis), Dopamine (physiology), Mesencephalon (metabolism), Mesencephalon (pathology), Mice, Mice, Inbred C57BL, Mice, Neurologic Mutants (metabolism), Nerve Degeneration, Nerve Tissue Proteins (analysis), Neurons (metabolism), Parkinson Disease (metabolism), Parkinson Disease (pathology), S100 Calcium Binding Protein G (metabolism), Substantia Nigra (metabolism), Substantia Nigra (pathology), Telencephalon (metabolism), Telencephalon (pathology), Tyrosine 3-Monooxygenase (analysis).
- MESH :
- chemical , analysis : Dopamine, Nerve Tissue Proteins, Tyrosine 3-Monooxygenase.
- chemical , metabolism : S100 Calcium Binding Protein G.
- chemical , physiology : Dopamine.
- chemical : Calbindin 1, Calbindins.
- chemistry : Cell Nucleus, Cytoplasm.
- metabolism : Corpus Striatum, Mesencephalon, Mice, Neurologic Mutants, Neurons, Parkinson Disease, Substantia Nigra, Telencephalon.
- pathology : Afferent Pathways, Corpus Striatum, Mesencephalon, Parkinson Disease, Substantia Nigra, Telencephalon.
- Animals, Disease Models, Animal, Mice, Mice, Inbred C57BL, Nerve Degeneration.
Abstract
In mice carrying the weaver mutation there is a spontaneous degeneration of dopaminergic neurons that is heterogeneous among cell groups: nigrostriatal neurons are more affected than mesolimbic neurons, while involvement of the mesocortical system is controversial. We questioned whether the pattern of cell loss in mesencephalon and fiber depletion in telencephalon could be related to the differential content of Calbindin-D28k in dopaminergic cells. The mesencephalon of seven-month-old mutants was serially sectioned and alternate series were immunostained with tyrosine hydroxylase and Calbindin-D28k. Cell counts indicated a 40% loss for the ensemble of dopamine mesencephalic neurons. However, double-immunostained preparations revealed that this cell loss was restricted to the neurons that lacked Calbindin-D28k, which were reduced by 72%, while the dopaminergic neurons containing Calbindin-D28k were completely spared. Calbindin-D28k was present in both the cytoplasm and nucleus of the dopaminergic cells. This nuclear localization was confirmed at the ultrastructural level. In the telencephalon of weaver mutants, areas receiving projections from the Calbindin-D28k-positive dopaminergic neurons, such as the cerebral cortex, contained normal densities of fibers, while areas harboring projections from the non-Calbindin-D28k dopaminergic neurons, such as the dorsal striatum, had reduced amounts of fibers. The vulnerability pattern in the mesencephalon of weaver mutants bears similarities to that described in idiopathic Parkinson's disease or in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonism: Calbindin-D28k may thus delimit a group of dopaminergic neurons resistant to cell death in different conditions. On the other hand, the vulnerability pattern of dopaminergic fibers in weaver differs from that of Parkinson's disease, since there is a complete sparing of the dopaminergic mesocortical projection in weaver, contrasting with the damage of these projections in Parkinson's disease.
PubMed: 7969910
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Sparing of the dopaminergic neurons containing calbindin-D28k and of the dopaminergic mesocortical projections in weaver mutant mice.</title><author><name sortKey="Gaspar, P" sort="Gaspar, P" uniqKey="Gaspar P" first="P" last="Gaspar">P. Gaspar</name><affiliation><nlm:affiliation>INSERM U 106, Batiment de Pédiatrie, Hôpital Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ben Jelloun, N" sort="Ben Jelloun, N" uniqKey="Ben Jelloun N" first="N" last="Ben Jelloun">N. Ben Jelloun</name></author><author><name sortKey="Febvret, A" sort="Febvret, A" uniqKey="Febvret A" first="A" last="Febvret">A. Febvret</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:7969910</idno><idno type="pmid">7969910</idno><idno type="wicri:Area/PubMed/Corpus">001675</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001675</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Sparing of the dopaminergic neurons containing calbindin-D28k and of the dopaminergic mesocortical projections in weaver mutant mice.</title><author><name sortKey="Gaspar, P" sort="Gaspar, P" uniqKey="Gaspar P" first="P" last="Gaspar">P. Gaspar</name><affiliation><nlm:affiliation>INSERM U 106, Batiment de Pédiatrie, Hôpital Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ben Jelloun, N" sort="Ben Jelloun, N" uniqKey="Ben Jelloun N" first="N" last="Ben Jelloun">N. Ben Jelloun</name></author><author><name sortKey="Febvret, A" sort="Febvret, A" uniqKey="Febvret A" first="A" last="Febvret">A. Febvret</name></author></analytic><series><title level="j">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Afferent Pathways (pathology)</term><term>Animals</term><term>Calbindin 1</term><term>Calbindins</term><term>Cell Nucleus (chemistry)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Cytoplasm (chemistry)</term><term>Disease Models, Animal</term><term>Dopamine (analysis)</term><term>Dopamine (physiology)</term><term>Mesencephalon (metabolism)</term><term>Mesencephalon (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Neurologic Mutants (metabolism)</term><term>Nerve Degeneration</term><term>Nerve Tissue Proteins (analysis)</term><term>Neurons (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>S100 Calcium Binding Protein G (metabolism)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Telencephalon (metabolism)</term><term>Telencephalon (pathology)</term><term>Tyrosine 3-Monooxygenase (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Dopamine</term><term>Nerve Tissue Proteins</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>S100 Calcium Binding Protein G</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Calbindin 1</term><term>Calbindins</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cell Nucleus</term><term>Cytoplasm</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Mesencephalon</term><term>Mice, Neurologic Mutants</term><term>Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Telencephalon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Afferent Pathways</term><term>Corpus Striatum</term><term>Mesencephalon</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Telencephalon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Nerve Degeneration</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In mice carrying the weaver mutation there is a spontaneous degeneration of dopaminergic neurons that is heterogeneous among cell groups: nigrostriatal neurons are more affected than mesolimbic neurons, while involvement of the mesocortical system is controversial. We questioned whether the pattern of cell loss in mesencephalon and fiber depletion in telencephalon could be related to the differential content of Calbindin-D28k in dopaminergic cells. The mesencephalon of seven-month-old mutants was serially sectioned and alternate series were immunostained with tyrosine hydroxylase and Calbindin-D28k. Cell counts indicated a 40% loss for the ensemble of dopamine mesencephalic neurons. However, double-immunostained preparations revealed that this cell loss was restricted to the neurons that lacked Calbindin-D28k, which were reduced by 72%, while the dopaminergic neurons containing Calbindin-D28k were completely spared. Calbindin-D28k was present in both the cytoplasm and nucleus of the dopaminergic cells. This nuclear localization was confirmed at the ultrastructural level. In the telencephalon of weaver mutants, areas receiving projections from the Calbindin-D28k-positive dopaminergic neurons, such as the cerebral cortex, contained normal densities of fibers, while areas harboring projections from the non-Calbindin-D28k dopaminergic neurons, such as the dorsal striatum, had reduced amounts of fibers. The vulnerability pattern in the mesencephalon of weaver mutants bears similarities to that described in idiopathic Parkinson's disease or in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonism: Calbindin-D28k may thus delimit a group of dopaminergic neurons resistant to cell death in different conditions. On the other hand, the vulnerability pattern of dopaminergic fibers in weaver differs from that of Parkinson's disease, since there is a complete sparing of the dopaminergic mesocortical projection in weaver, contrasting with the damage of these projections in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7969910</PMID><DateCreated><Year>1994</Year><Month>12</Month><Day>08</Day></DateCreated><DateCompleted><Year>1994</Year><Month>12</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0306-4522</ISSN><JournalIssue CitedMedium="Print"><Volume>61</Volume><Issue>2</Issue><PubDate><Year>1994</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Neuroscience</Title><ISOAbbreviation>Neuroscience</ISOAbbreviation></Journal><ArticleTitle>Sparing of the dopaminergic neurons containing calbindin-D28k and of the dopaminergic mesocortical projections in weaver mutant mice.</ArticleTitle><Pagination><MedlinePgn>293-305</MedlinePgn></Pagination><Abstract><AbstractText>In mice carrying the weaver mutation there is a spontaneous degeneration of dopaminergic neurons that is heterogeneous among cell groups: nigrostriatal neurons are more affected than mesolimbic neurons, while involvement of the mesocortical system is controversial. We questioned whether the pattern of cell loss in mesencephalon and fiber depletion in telencephalon could be related to the differential content of Calbindin-D28k in dopaminergic cells. The mesencephalon of seven-month-old mutants was serially sectioned and alternate series were immunostained with tyrosine hydroxylase and Calbindin-D28k. Cell counts indicated a 40% loss for the ensemble of dopamine mesencephalic neurons. However, double-immunostained preparations revealed that this cell loss was restricted to the neurons that lacked Calbindin-D28k, which were reduced by 72%, while the dopaminergic neurons containing Calbindin-D28k were completely spared. Calbindin-D28k was present in both the cytoplasm and nucleus of the dopaminergic cells. This nuclear localization was confirmed at the ultrastructural level. In the telencephalon of weaver mutants, areas receiving projections from the Calbindin-D28k-positive dopaminergic neurons, such as the cerebral cortex, contained normal densities of fibers, while areas harboring projections from the non-Calbindin-D28k dopaminergic neurons, such as the dorsal striatum, had reduced amounts of fibers. The vulnerability pattern in the mesencephalon of weaver mutants bears similarities to that described in idiopathic Parkinson's disease or in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonism: Calbindin-D28k may thus delimit a group of dopaminergic neurons resistant to cell death in different conditions. On the other hand, the vulnerability pattern of dopaminergic fibers in weaver differs from that of Parkinson's disease, since there is a complete sparing of the dopaminergic mesocortical projection in weaver, contrasting with the damage of these projections in Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gaspar</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>INSERM U 106, Batiment de Pédiatrie, Hôpital Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ben Jelloun</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Febvret</LastName><ForeName>A</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscience</MedlineTA><NlmUniqueID>7605074</NlmUniqueID><ISSNLinking>0306-4522</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C576499">Calb1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064092">Calbindin 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064026">Calbindins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064030">S100 Calcium Binding Protein G</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance 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