Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism.
Identifieur interne : 000D60 ( PubMed/Corpus ); précédent : 000D59; suivant : 000D61Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism.
Auteurs : Arthur Leblois ; Wassilios Meissner ; Bernard Bioulac ; Christian E. Gross ; David Hansel ; Thomas BoraudSource :
- The European journal of neuroscience [ 0953-816X ] ; 2007.
English descriptors
- KwdEn :
- Algorithms, Animals, Basal Ganglia (physiology), Behavior, Animal (physiology), Cortical Synchronization, Disease Progression, Electrophysiology, Female, Globus Pallidus (cytology), Globus Pallidus (physiology), MPTP Poisoning (physiopathology), Macaca mulatta, Movement (physiology), Neurons (physiology), Parkinson Disease, Secondary (physiopathology), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Tyrosine 3-Monooxygenase.
- cytology : Globus Pallidus.
- physiology : Basal Ganglia, Behavior, Animal, Globus Pallidus, Movement, Neurons.
- physiopathology : MPTP Poisoning, Parkinson Disease, Secondary.
- Algorithms, Animals, Cortical Synchronization, Disease Progression, Electrophysiology, Female, Macaca mulatta.
Abstract
Parkinson's disease is known to result from basal ganglia dysfunction. Electrophysiological recordings in parkinsonian patients and animals have shown the emergence of abnormal synchronous oscillatory activity in the cortico-basal ganglia network in the pathological condition. In addition, previous studies pointed out an altered response pattern during movement execution in the pallidum of parkinsonian animals. To investigate the dynamics of these changes during disease progression and to relate them to the onset of the motor symptoms, we recorded spontaneous and movement-related neuronal activity in the internal pallidum of nonhuman primates during a progressive dopamine depletion process. Parkinsonian motor symptoms appeared progressively during the intoxication protocol, at the end of which both animals displayed severe akinesia, rigidity and postural abnormalities. Spontaneous firing rates did not vary significantly after intoxication. During the early phase of the protocol, voluntary movements were significantly slowed down and delayed. At the same time, the neuronal response to movement execution was modified and inhibitory responses disappeared. In contrast, the unitary and collective dynamic properties of spontaneous neuronal activity, as revealed by spectral and correlation analysis, remained unchanged during this period. Spontaneous correlated activity increased later, after animals became severely bradykinetic, whereas synchronous oscillatory activity appeared only after major motor symptoms developed. Thus, a causality between the emergence of synchronous oscillations in the pallidum and main parkinsonian motor symptoms seems unlikely. The pathological disruption of movement-related activity in the basal ganglia appears to be a better correlate at least to bradykinesia and stands as the best candidate to account for this motor symptom.
DOI: 10.1111/j.1460-9568.2007.05777.x
PubMed: 17880401
Links to Exploration step
pubmed:17880401Le document en format XML
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Gross</name></author><author><name sortKey="Hansel, David" sort="Hansel, David" uniqKey="Hansel D" first="David" last="Hansel">David Hansel</name></author><author><name sortKey="Boraud, Thomas" sort="Boraud, Thomas" uniqKey="Boraud T" first="Thomas" last="Boraud">Thomas Boraud</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17880401</idno><idno type="pmid">17880401</idno><idno type="doi">10.1111/j.1460-9568.2007.05777.x</idno><idno type="wicri:Area/PubMed/Corpus">000D60</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D60</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism.</title><author><name sortKey="Leblois, Arthur" sort="Leblois, Arthur" uniqKey="Leblois A" first="Arthur" last="Leblois">Arthur Leblois</name><affiliation><nlm:affiliation>Université Bordeaux 2, UMR CNRS 5227 Laboratoire Motricite Adaptation Cognition, Basal Gang, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. aleblois@yahoo.fr</nlm:affiliation></affiliation></author><author><name sortKey="Meissner, Wassilios" sort="Meissner, Wassilios" uniqKey="Meissner W" first="Wassilios" last="Meissner">Wassilios Meissner</name></author><author><name sortKey="Bioulac, Bernard" sort="Bioulac, Bernard" uniqKey="Bioulac B" first="Bernard" last="Bioulac">Bernard Bioulac</name></author><author><name sortKey="Gross, Christian E" sort="Gross, Christian E" uniqKey="Gross C" first="Christian E" last="Gross">Christian E. Gross</name></author><author><name sortKey="Hansel, David" sort="Hansel, David" uniqKey="Hansel D" first="David" last="Hansel">David Hansel</name></author><author><name sortKey="Boraud, Thomas" sort="Boraud, Thomas" uniqKey="Boraud T" first="Thomas" last="Boraud">Thomas Boraud</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Algorithms</term><term>Animals</term><term>Basal Ganglia (physiology)</term><term>Behavior, Animal (physiology)</term><term>Cortical Synchronization</term><term>Disease Progression</term><term>Electrophysiology</term><term>Female</term><term>Globus Pallidus (cytology)</term><term>Globus Pallidus (physiology)</term><term>MPTP Poisoning (physiopathology)</term><term>Macaca mulatta</term><term>Movement (physiology)</term><term>Neurons (physiology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Globus Pallidus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Basal Ganglia</term><term>Behavior, Animal</term><term>Globus Pallidus</term><term>Movement</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>MPTP Poisoning</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Algorithms</term><term>Animals</term><term>Cortical Synchronization</term><term>Disease Progression</term><term>Electrophysiology</term><term>Female</term><term>Macaca mulatta</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is known to result from basal ganglia dysfunction. Electrophysiological recordings in parkinsonian patients and animals have shown the emergence of abnormal synchronous oscillatory activity in the cortico-basal ganglia network in the pathological condition. In addition, previous studies pointed out an altered response pattern during movement execution in the pallidum of parkinsonian animals. To investigate the dynamics of these changes during disease progression and to relate them to the onset of the motor symptoms, we recorded spontaneous and movement-related neuronal activity in the internal pallidum of nonhuman primates during a progressive dopamine depletion process. Parkinsonian motor symptoms appeared progressively during the intoxication protocol, at the end of which both animals displayed severe akinesia, rigidity and postural abnormalities. Spontaneous firing rates did not vary significantly after intoxication. During the early phase of the protocol, voluntary movements were significantly slowed down and delayed. At the same time, the neuronal response to movement execution was modified and inhibitory responses disappeared. In contrast, the unitary and collective dynamic properties of spontaneous neuronal activity, as revealed by spectral and correlation analysis, remained unchanged during this period. Spontaneous correlated activity increased later, after animals became severely bradykinetic, whereas synchronous oscillatory activity appeared only after major motor symptoms developed. Thus, a causality between the emergence of synchronous oscillations in the pallidum and main parkinsonian motor symptoms seems unlikely. The pathological disruption of movement-related activity in the basal ganglia appears to be a better correlate at least to bradykinesia and stands as the best candidate to account for this motor symptom.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17880401</PMID><DateCreated><Year>2007</Year><Month>09</Month><Day>20</Day></DateCreated><DateCompleted><Year>2007</Year><Month>11</Month><Day>20</Day></DateCompleted><DateRevised><Year>2007</Year><Month>09</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-816X</ISSN><JournalIssue CitedMedium="Print"><Volume>26</Volume><Issue>6</Issue><PubDate><Year>2007</Year><Month>Sep</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism.</ArticleTitle><Pagination><MedlinePgn>1701-13</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease is known to result from basal ganglia dysfunction. Electrophysiological recordings in parkinsonian patients and animals have shown the emergence of abnormal synchronous oscillatory activity in the cortico-basal ganglia network in the pathological condition. In addition, previous studies pointed out an altered response pattern during movement execution in the pallidum of parkinsonian animals. To investigate the dynamics of these changes during disease progression and to relate them to the onset of the motor symptoms, we recorded spontaneous and movement-related neuronal activity in the internal pallidum of nonhuman primates during a progressive dopamine depletion process. Parkinsonian motor symptoms appeared progressively during the intoxication protocol, at the end of which both animals displayed severe akinesia, rigidity and postural abnormalities. Spontaneous firing rates did not vary significantly after intoxication. During the early phase of the protocol, voluntary movements were significantly slowed down and delayed. At the same time, the neuronal response to movement execution was modified and inhibitory responses disappeared. In contrast, the unitary and collective dynamic properties of spontaneous neuronal activity, as revealed by spectral and correlation analysis, remained unchanged during this period. Spontaneous correlated activity increased later, after animals became severely bradykinetic, whereas synchronous oscillatory activity appeared only after major motor symptoms developed. Thus, a causality between the emergence of synchronous oscillations in the pallidum and main parkinsonian motor symptoms seems unlikely. The pathological disruption of movement-related activity in the basal ganglia appears to be a better correlate at least to bradykinesia and stands as the best candidate to account for this motor symptom.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leblois</LastName><ForeName>Arthur</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Université Bordeaux 2, UMR CNRS 5227 Laboratoire Motricite Adaptation Cognition, Basal Gang, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. aleblois@yahoo.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meissner</LastName><ForeName>Wassilios</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Bioulac</LastName><ForeName>Bernard</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gross</LastName><ForeName>Christian E</ForeName><Initials>CE</Initials></Author><Author ValidYN="Y"><LastName>Hansel</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Boraud</LastName><ForeName>Thomas</ForeName><Initials>T</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>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003344" MajorTopicYN="Y">Cortical Synchronization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004594" MajorTopicYN="N">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020267" MajorTopicYN="N">MPTP Poisoning</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008253" MajorTopicYN="N">Macaca mulatta</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>9</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>12</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>9</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17880401</ArticleId><ArticleId IdType="pii">EJN5777</ArticleId><ArticleId IdType="doi">10.1111/j.1460-9568.2007.05777.x</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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