Dopamine depletion impairs precursor cell proliferation in Parkinson disease.
Identifieur interne : 001011 ( PubMed/Corpus ); précédent : 001010; suivant : 001012Dopamine depletion impairs precursor cell proliferation in Parkinson disease.
Auteurs : Günter U. Höglinger ; Pamela Rizk ; Marie P. Muriel ; Charles Duyckaerts ; Wolfgang H. Oertel ; Isabelle Caille ; Etienne C. HirschSource :
- Nature neuroscience [ 1097-6256 ] ; 2004.
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Animals, Antiparkinson Agents (therapeutic use), Bromodeoxyuridine (metabolism), Case-Control Studies, Cell Count (methods), Cell Death (physiology), Cell Division (drug effects), Cells, Cultured, Dopamine (deficiency), Dopamine (physiology), Dopamine Antagonists (pharmacology), Dopamine Plasma Membrane Transport Proteins, Drug Interactions, Ependyma (ultrastructure), Female, Glial Fibrillary Acidic Protein (metabolism), Glycoproteins (metabolism), Humans, Immunohistochemistry (methods), In Situ Nick-End Labeling (methods), Indoles (therapeutic use), Intermediate Filament Proteins (metabolism), Levodopa (therapeutic use), Male, Membrane Glycoproteins (metabolism), Membrane Transport Proteins (metabolism), Mice, Mice, Inbred C57BL, Microscopy, Confocal (methods), Microscopy, Immunoelectron (methods), Microspheres, Middle Aged, Nerve Tissue Proteins (metabolism), Nestin, Neural Cell Adhesion Molecule L1 (metabolism), Neurons (metabolism), Neurons (pathology), Neurons (ultrastructure), Olfactory Bulb (cytology), Olfactory Bulb (metabolism), Oxidopamine (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Postmortem Changes, Rats, Rats, Sprague-Dawley, Receptor, Epidermal Growth Factor, Receptor, ErbB-2, Receptors, Dopamine (metabolism), Sialic Acids (metabolism), Stem Cells (metabolism), Stem Cells (pathology), Stem Cells (ultrastructure), Time Factors, Tubulin (metabolism), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , deficiency : Dopamine.
- chemical , metabolism : Bromodeoxyuridine, Glial Fibrillary Acidic Protein, Glycoproteins, Intermediate Filament Proteins, Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins, Neural Cell Adhesion Molecule L1, Receptors, Dopamine, Sialic Acids, Tubulin, Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Dopamine Antagonists.
- chemical , physiology : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Indoles, Levodopa.
- cytology : Olfactory Bulb.
- drug effects : Cell Division.
- drug therapy : Parkinson Disease.
- metabolism : Neurons, Olfactory Bulb, Parkinson Disease, Parkinsonian Disorders, Stem Cells.
- methods : Cell Count, Immunohistochemistry, In Situ Nick-End Labeling, Microscopy, Confocal, Microscopy, Immunoelectron.
- pathology : Neurons, Parkinson Disease, Parkinsonian Disorders, Stem Cells.
- physiology : Cell Death.
- chemical , toxicity : Oxidopamine.
- ultrastructure : Ependyma, Neurons, Stem Cells.
- Aged, Analysis of Variance, Animals, Case-Control Studies, Cells, Cultured, Dopamine Plasma Membrane Transport Proteins, Drug Interactions, Female, Humans, Male, Mice, Mice, Inbred C57BL, Microspheres, Middle Aged, Nestin, Postmortem Changes, Rats, Rats, Sprague-Dawley, Receptor, Epidermal Growth Factor, Receptor, ErbB-2, Time Factors.
Abstract
Cerebral dopamine depletion is the hallmark of Parkinson disease. Because dopamine modulates ontogenetic neurogenesis, depletion of dopamine might affect neural precursors in the subependymal zone and subgranular zone of the adult brain. Here we provide ultrastructural evidence showing that highly proliferative precursors in the adult subependymal zone express dopamine receptors and receive dopaminergic afferents. Experimental depletion of dopamine in rodents decreases precursor cell proliferation in both the subependymal zone and the subgranular zone. Proliferation is restored completely by a selective agonist of D2-like (D2L) receptors. Experiments with neural precursors from the adult subependymal zone grown as neurosphere cultures confirm that activation of D2L receptors directly increases the proliferation of these precursors. Consistently, the numbers of proliferating cells in the subependymal zone and neural precursor cells in the subgranular zone and olfactory bulb are reduced in postmortem brains of individuals with Parkinson disease. These observations suggest that the generation of neural precursor cells is impaired in Parkinson disease as a consequence of dopaminergic denervation.
DOI: 10.1038/nn1265
PubMed: 15195095
Links to Exploration step
pubmed:15195095Le document en format XML
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Muriel</name></author><author><name sortKey="Duyckaerts, Charles" sort="Duyckaerts, Charles" uniqKey="Duyckaerts C" first="Charles" last="Duyckaerts">Charles Duyckaerts</name></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H" last="Oertel">Wolfgang H. Oertel</name></author><author><name sortKey="Caille, Isabelle" sort="Caille, Isabelle" uniqKey="Caille I" first="Isabelle" last="Caille">Isabelle Caille</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. 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Because dopamine modulates ontogenetic neurogenesis, depletion of dopamine might affect neural precursors in the subependymal zone and subgranular zone of the adult brain. Here we provide ultrastructural evidence showing that highly proliferative precursors in the adult subependymal zone express dopamine receptors and receive dopaminergic afferents. Experimental depletion of dopamine in rodents decreases precursor cell proliferation in both the subependymal zone and the subgranular zone. Proliferation is restored completely by a selective agonist of D2-like (D2L) receptors. Experiments with neural precursors from the adult subependymal zone grown as neurosphere cultures confirm that activation of D2L receptors directly increases the proliferation of these precursors. Consistently, the numbers of proliferating cells in the subependymal zone and neural precursor cells in the subgranular zone and olfactory bulb are reduced in postmortem brains of individuals with Parkinson disease. These observations suggest that the generation of neural precursor cells is impaired in Parkinson disease as a consequence of dopaminergic denervation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15195095</PMID><DateCreated><Year>2004</Year><Month>06</Month><Day>28</Day></DateCreated><DateCompleted><Year>2004</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1097-6256</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><Issue>7</Issue><PubDate><Year>2004</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Nature neuroscience</Title><ISOAbbreviation>Nat. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Dopamine depletion impairs precursor cell proliferation in Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>726-35</MedlinePgn></Pagination><Abstract><AbstractText>Cerebral dopamine depletion is the hallmark of Parkinson disease. Because dopamine modulates ontogenetic neurogenesis, depletion of dopamine might affect neural precursors in the subependymal zone and subgranular zone of the adult brain. Here we provide ultrastructural evidence showing that highly proliferative precursors in the adult subependymal zone express dopamine receptors and receive dopaminergic afferents. Experimental depletion of dopamine in rodents decreases precursor cell proliferation in both the subependymal zone and the subgranular zone. Proliferation is restored completely by a selective agonist of D2-like (D2L) receptors. Experiments with neural precursors from the adult subependymal zone grown as neurosphere cultures confirm that activation of D2L receptors directly increases the proliferation of these precursors. Consistently, the numbers of proliferating cells in the subependymal zone and neural precursor cells in the subgranular zone and olfactory bulb are reduced in postmortem brains of individuals with Parkinson disease. These observations suggest that the generation of neural precursor cells is impaired in Parkinson disease as a consequence of dopaminergic denervation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Höglinger</LastName><ForeName>Günter U</ForeName><Initials>GU</Initials><AffiliationInfo><Affiliation>INSERM U289 Hôpital de la Salpetrière, F-75651 Paris, France. gunter@ccr.jussieu.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rizk</LastName><ForeName>Pamela</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Muriel</LastName><ForeName>Marie P</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>Duyckaerts</LastName><ForeName>Charles</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Oertel</LastName><ForeName>Wolfgang H</ForeName><Initials>WH</Initials></Author><Author ValidYN="Y"><LastName>Caille</LastName><ForeName>Isabelle</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2004</Year><Month>06</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Nat Neurosci</MedlineTA><NlmUniqueID>9809671</NlmUniqueID><ISSNLinking>1097-6256</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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PubStatus="medline"><Year>2004</Year><Month>9</Month><Day>15</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>6</Month><Day>15</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15195095</ArticleId><ArticleId IdType="doi">10.1038/nn1265</ArticleId><ArticleId IdType="pii">nn1265</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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