Involvement of the subthalamic nucleus in glutamatergic compensatory mechanisms.
Identifieur interne : 001402 ( PubMed/Corpus ); précédent : 001401; suivant : 001403Involvement of the subthalamic nucleus in glutamatergic compensatory mechanisms.
Auteurs : E. Bezard ; T. Boraud ; B. Bioulac ; C E GrossSource :
- The European journal of neuroscience [ 0953-816X ] ; 1999.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Adaptation, Physiological (physiology), Animals, Dopamine Agents, Electrophysiology, Globus Pallidus (physiopathology), Glutamic Acid (physiology), Macaca fascicularis, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Thalamic Nuclei (physiopathology).
- MESH :
- chemical , physiology : Glutamic Acid.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- physiology : Adaptation, Physiological.
- physiopathology : Globus Pallidus, Parkinson Disease, Secondary, Thalamic Nuclei.
- Animals, Electrophysiology, Macaca fascicularis.
Abstract
The purpose of the present study was to investigate whether the subthalamic nucleus (STN) was implicated in the glutamatergic compensatory mechanisms which have been shown to mask the parkinsonian motor abnormalities at the end of the presymptomatic period in experimental parkinsonism. Using multiunit electrophysiological recordings, we follow changes of activity occurring in the STN and in both the pars externalis and the pars internalis of the globus pallidus of monkeys chronically intoxicated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), according to a protocol designed to mimic the gradual evolution of dopaminergic neuronal death. STN activity augmented significantly in the course of treatment, even before the first appearance of clinical signs (P < 0.01). This result would indicate that the STN, which increases its level of activity even before the end of the presymptomatic period, is principally responsible for the instigation of glutamatergic compensatory mechanisms which allow the maintenance of the striatal dopaminergic homeostasis.
PubMed: 10336685
Links to Exploration step
pubmed:10336685Le document en format XML
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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="1999">1999</date><idno type="RBID">pubmed:10336685</idno><idno type="pmid">10336685</idno><idno type="wicri:Area/PubMed/Corpus">001402</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001402</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Involvement of the subthalamic nucleus in glutamatergic compensatory mechanisms.</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. erwan.bezard@umr5543.u-bordeaux2.fr</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">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Adaptation, Physiological (physiology)</term><term>Animals</term><term>Dopamine Agents</term><term>Electrophysiology</term><term>Globus Pallidus (physiopathology)</term><term>Glutamic Acid (physiology)</term><term>Macaca fascicularis</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Thalamic Nuclei (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glutamic Acid</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Adaptation, Physiological</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Globus Pallidus</term><term>Parkinson Disease, Secondary</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Electrophysiology</term><term>Macaca fascicularis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The purpose of the present study was to investigate whether the subthalamic nucleus (STN) was implicated in the glutamatergic compensatory mechanisms which have been shown to mask the parkinsonian motor abnormalities at the end of the presymptomatic period in experimental parkinsonism. Using multiunit electrophysiological recordings, we follow changes of activity occurring in the STN and in both the pars externalis and the pars internalis of the globus pallidus of monkeys chronically intoxicated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), according to a protocol designed to mimic the gradual evolution of dopaminergic neuronal death. STN activity augmented significantly in the course of treatment, even before the first appearance of clinical signs (P < 0.01). This result would indicate that the STN, which increases its level of activity even before the end of the presymptomatic period, is principally responsible for the instigation of glutamatergic compensatory mechanisms which allow the maintenance of the striatal dopaminergic homeostasis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10336685</PMID><DateCreated><Year>1999</Year><Month>07</Month><Day>01</Day></DateCreated><DateCompleted><Year>1999</Year><Month>07</Month><Day>01</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-816X</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>6</Issue><PubDate><Year>1999</Year><Month>Jun</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Involvement of the subthalamic nucleus in glutamatergic compensatory mechanisms.</ArticleTitle><Pagination><MedlinePgn>2167-70</MedlinePgn></Pagination><Abstract><AbstractText>The purpose of the present study was to investigate whether the subthalamic nucleus (STN) was implicated in the glutamatergic compensatory mechanisms which have been shown to mask the parkinsonian motor abnormalities at the end of the presymptomatic period in experimental parkinsonism. Using multiunit electrophysiological recordings, we follow changes of activity occurring in the STN and in both the pars externalis and the pars internalis of the globus pallidus of monkeys chronically intoxicated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), according to a protocol designed to mimic the gradual evolution of dopaminergic neuronal death. STN activity augmented significantly in the course of treatment, even before the first appearance of clinical signs (P < 0.01). This result would indicate that the STN, which increases its level of activity even before the end of the presymptomatic period, is principally responsible for the instigation of glutamatergic compensatory mechanisms which allow the maintenance of the striatal dopaminergic homeostasis.</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. erwan.bezard@umr5543.u-bordeaux2.fr</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>France</Country><MedlineTA>Eur J Neurosci</MedlineTA><NlmUniqueID>8918110</NlmUniqueID><ISSNLinking>0953-816X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>3KX376GY7L</RegistryNumber><NameOfSubstance UI="D018698">Glutamic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="N">Adaptation, Physiological</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="N">Dopamine Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004594" MajorTopicYN="N">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018698" MajorTopicYN="N">Glutamic Acid</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013787" MajorTopicYN="N">Thalamic Nuclei</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>5</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>5</Month><Day>21</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>5</Month><Day>21</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10336685</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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