Presymptomatic revelation of experimental parkinsonism.
Identifieur interne : 001542 ( PubMed/Corpus ); précédent : 001541; suivant : 001543Presymptomatic revelation of experimental parkinsonism.
Auteurs : E. Bezard ; T. Boraud ; B. Bioulac ; C E GrossSource :
- Neuroreport [ 0959-4965 ] ; 1997.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Kynurenic Acid.
- drug effects : Behavior, Animal.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Macaca.
Abstract
Parkinson's disease results from a progressive loss of dopaminergic neurones of the substantia nigra (SNc). Clinical symptoms only appear, however, when neuronal death exceeds 50-60%: their late appearance is due to compensatory mechanisms. The possibility exists that glutamatergic inputs to the SNc may be implicated in this 'masking' of the disease. To test this hypothesis, we evaluated the effects of reversible pharmacological blockage of these inputs in asymptomatic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. The result was the appearance of motor disturbances. This finding supports the idea that SNc glutamatergic inputs are largely involved in compensatory mechanisms during presymptomatic period. Blockade of these inputs could lead to presymptomatic diagnosis of Parkinson's disease.
PubMed: 9080424
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Bioulac</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9080424</idno><idno type="pmid">9080424</idno><idno type="wicri:Area/PubMed/Corpus">001542</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001542</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Presymptomatic revelation of experimental parkinsonism.</title><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France.</nlm:affiliation></affiliation></author><author><name sortKey="Boraud, T" sort="Boraud, T" uniqKey="Boraud T" first="T" last="Boraud">T. Boraud</name></author><author><name sortKey="Bioulac, B" sort="Bioulac, B" uniqKey="Bioulac B" first="B" last="Bioulac">B. Bioulac</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">Neuroreport</title><idno type="ISSN">0959-4965</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Animals</term><term>Behavior, Animal (drug effects)</term><term>Disease Models, Animal</term><term>Kynurenic Acid (pharmacology)</term><term>Macaca</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Kynurenic Acid</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Macaca</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease results from a progressive loss of dopaminergic neurones of the substantia nigra (SNc). Clinical symptoms only appear, however, when neuronal death exceeds 50-60%: their late appearance is due to compensatory mechanisms. The possibility exists that glutamatergic inputs to the SNc may be implicated in this 'masking' of the disease. To test this hypothesis, we evaluated the effects of reversible pharmacological blockage of these inputs in asymptomatic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. The result was the appearance of motor disturbances. This finding supports the idea that SNc glutamatergic inputs are largely involved in compensatory mechanisms during presymptomatic period. Blockade of these inputs could lead to presymptomatic diagnosis of Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9080424</PMID><DateCreated><Year>1997</Year><Month>06</Month><Day>13</Day></DateCreated><DateCompleted><Year>1997</Year><Month>06</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0959-4965</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><Issue>2</Issue><PubDate><Year>1997</Year><Month>Jan</Month><Day>20</Day></PubDate></JournalIssue><Title>Neuroreport</Title><ISOAbbreviation>Neuroreport</ISOAbbreviation></Journal><ArticleTitle>Presymptomatic revelation of experimental parkinsonism.</ArticleTitle><Pagination><MedlinePgn>435-8</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease results from a progressive loss of dopaminergic neurones of the substantia nigra (SNc). Clinical symptoms only appear, however, when neuronal death exceeds 50-60%: their late appearance is due to compensatory mechanisms. The possibility exists that glutamatergic inputs to the SNc may be implicated in this 'masking' of the disease. To test this hypothesis, we evaluated the effects of reversible pharmacological blockage of these inputs in asymptomatic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. The result was the appearance of motor disturbances. This finding supports the idea that SNc glutamatergic inputs are largely involved in compensatory mechanisms during presymptomatic period. Blockade of these inputs could lead to presymptomatic diagnosis of Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boraud</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Bioulac</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gross</LastName><ForeName>C E</ForeName><Initials>CE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Neuroreport</MedlineTA><NlmUniqueID>9100935</NlmUniqueID><ISSNLinking>0959-4965</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>H030S2S85J</RegistryNumber><NameOfSubstance UI="D007736">Kynurenic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007736" MajorTopicYN="N">Kynurenic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008251" MajorTopicYN="N">Macaca</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>1</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>1</Month><Day>20</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>1</Month><Day>20</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9080424</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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