Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.
Identifieur interne : 001506 ( PubMed/Corpus ); précédent : 001505; suivant : 001507Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.
Auteurs : Ron Levy ; Peter Ashby ; William D. Hutchison ; Anthony E. Lang ; Andres M. Lozano ; Jonathan O. DostrovskySource :
- Brain : a journal of neurology [ 0006-8950 ] ; 2002.
English descriptors
- KwdEn :
- Action Potentials (drug effects), Action Potentials (physiology), Adult, Aged, Biological Clocks (drug effects), Biological Clocks (physiology), Dopamine (physiology), Dopamine Agents (pharmacology), Dopamine Agents (therapeutic use), Female, Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Male, Middle Aged, Monitoring, Intraoperative (methods), Monitoring, Intraoperative (statistics & numerical data), Movement (drug effects), Movement (physiology), Neurons (drug effects), Neurons (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Subthalamic Nucleus (drug effects), Subthalamic Nucleus (physiology).
- MESH :
- chemical , pharmacology : Dopamine Agents, Levodopa.
- chemical , physiology : Dopamine.
- drug effects : Action Potentials, Biological Clocks, Movement, Neurons, Subthalamic Nucleus.
- drug therapy : Parkinson Disease.
- methods : Monitoring, Intraoperative.
- physiology : Action Potentials, Biological Clocks, Movement, Neurons, Subthalamic Nucleus.
- physiopathology : Parkinson Disease.
- statistics & numerical data : Monitoring, Intraoperative.
- chemical , therapeutic use : Dopamine Agents, Levodopa.
- Adult, Aged, Female, Humans, Male, Middle Aged.
Abstract
Local field potentials and pairs of neurones in the subthalamic nucleus (STN) of patients with Parkinson's disease show high-frequency oscillations (HFOs) at 15-30 Hz. This study explores how these HFOs are modulated by voluntary movements and by dopaminergic medication. We examined 15 patients undergoing implantation of bilateral deep brain stimulating electrodes using microelectrode recordings of pairs of STN neurones (eight patients) and macroelectrode recordings of local field potentials from the STN (14 patients). Synchronized HFOs between STN neurones were observed in 28 out of 37 pairs in five patients who had tremor in the operating room and none of 45 pairs in three patients who did not. In two of the three non-tremulous patients, HFOs in the frequency spectra of local field potentials were detected but were weaker than in those patients with tremor. Active movement suppressed synchronized HFOs in three out of five pairs of neurones, independent of changes in firing rate. HFOs observed in the local field potentials in nine out of 14 patients were reduced with voluntary movement in six of the eight patients tested. Dopaminergic medication decreased the incidence of synchronized HFOs in STN neurone pairs, reduced HFO synchrony in a pair of tremor cells concurrent with a reduction in firing rate and limb tremor, and decreased HFOs of local field potentials in the STN. These results demonstrate that HFO synchronization in the STN is reduced by voluntary movements and by exogenous dopaminergic medication. A mechanism for neuronal oscillatory synchronization in basal ganglia is proposed. It is suggested that the firing of STN neurones can be synchronized by 15-30 Hz cortical beta oscillatory activity, particularly when dopamine deficiency results in a higher background firing rate of STN neurones, and that this synchronization contributes to parkinsonian pathophysiology.
PubMed: 12023310
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Lozano</name></author><author><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O" last="Dostrovsky">Jonathan O. Dostrovsky</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12023310</idno><idno type="pmid">12023310</idno><idno type="wicri:Area/PubMed/Corpus">001506</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001506</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.</title><author><name sortKey="Levy, Ron" sort="Levy, Ron" uniqKey="Levy R" first="Ron" last="Levy">Ron Levy</name><affiliation><nlm:affiliation>Department of Physiology, University of Toronto, Toronto, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Ashby, Peter" sort="Ashby, Peter" uniqKey="Ashby P" first="Peter" last="Ashby">Peter Ashby</name></author><author><name sortKey="Hutchison, William D" sort="Hutchison, William D" uniqKey="Hutchison W" first="William D" last="Hutchison">William D. Hutchison</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name></author><author><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M" last="Lozano">Andres M. Lozano</name></author><author><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O" last="Dostrovsky">Jonathan O. Dostrovsky</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (drug effects)</term><term>Action Potentials (physiology)</term><term>Adult</term><term>Aged</term><term>Biological Clocks (drug effects)</term><term>Biological Clocks (physiology)</term><term>Dopamine (physiology)</term><term>Dopamine Agents (pharmacology)</term><term>Dopamine Agents (therapeutic use)</term><term>Female</term><term>Humans</term><term>Levodopa (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Monitoring, Intraoperative (methods)</term><term>Monitoring, Intraoperative (statistics & numerical data)</term><term>Movement (drug effects)</term><term>Movement (physiology)</term><term>Neurons (drug effects)</term><term>Neurons (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Subthalamic Nucleus (drug effects)</term><term>Subthalamic Nucleus (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</term><term>Biological Clocks</term><term>Movement</term><term>Neurons</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Monitoring, Intraoperative</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Biological Clocks</term><term>Movement</term><term>Neurons</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="statistics & numerical data" xml:lang="en"><term>Monitoring, Intraoperative</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Local field potentials and pairs of neurones in the subthalamic nucleus (STN) of patients with Parkinson's disease show high-frequency oscillations (HFOs) at 15-30 Hz. This study explores how these HFOs are modulated by voluntary movements and by dopaminergic medication. We examined 15 patients undergoing implantation of bilateral deep brain stimulating electrodes using microelectrode recordings of pairs of STN neurones (eight patients) and macroelectrode recordings of local field potentials from the STN (14 patients). Synchronized HFOs between STN neurones were observed in 28 out of 37 pairs in five patients who had tremor in the operating room and none of 45 pairs in three patients who did not. In two of the three non-tremulous patients, HFOs in the frequency spectra of local field potentials were detected but were weaker than in those patients with tremor. Active movement suppressed synchronized HFOs in three out of five pairs of neurones, independent of changes in firing rate. HFOs observed in the local field potentials in nine out of 14 patients were reduced with voluntary movement in six of the eight patients tested. Dopaminergic medication decreased the incidence of synchronized HFOs in STN neurone pairs, reduced HFO synchrony in a pair of tremor cells concurrent with a reduction in firing rate and limb tremor, and decreased HFOs of local field potentials in the STN. These results demonstrate that HFO synchronization in the STN is reduced by voluntary movements and by exogenous dopaminergic medication. A mechanism for neuronal oscillatory synchronization in basal ganglia is proposed. It is suggested that the firing of STN neurones can be synchronized by 15-30 Hz cortical beta oscillatory activity, particularly when dopamine deficiency results in a higher background firing rate of STN neurones, and that this synchronization contributes to parkinsonian pathophysiology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12023310</PMID><DateCreated><Year>2002</Year><Month>05</Month><Day>22</Day></DateCreated><DateCompleted><Year>2002</Year><Month>07</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8950</ISSN><JournalIssue CitedMedium="Print"><Volume>125</Volume><Issue>Pt 6</Issue><PubDate><Year>2002</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1196-209</MedlinePgn></Pagination><Abstract><AbstractText>Local field potentials and pairs of neurones in the subthalamic nucleus (STN) of patients with Parkinson's disease show high-frequency oscillations (HFOs) at 15-30 Hz. This study explores how these HFOs are modulated by voluntary movements and by dopaminergic medication. We examined 15 patients undergoing implantation of bilateral deep brain stimulating electrodes using microelectrode recordings of pairs of STN neurones (eight patients) and macroelectrode recordings of local field potentials from the STN (14 patients). Synchronized HFOs between STN neurones were observed in 28 out of 37 pairs in five patients who had tremor in the operating room and none of 45 pairs in three patients who did not. In two of the three non-tremulous patients, HFOs in the frequency spectra of local field potentials were detected but were weaker than in those patients with tremor. Active movement suppressed synchronized HFOs in three out of five pairs of neurones, independent of changes in firing rate. HFOs observed in the local field potentials in nine out of 14 patients were reduced with voluntary movement in six of the eight patients tested. Dopaminergic medication decreased the incidence of synchronized HFOs in STN neurone pairs, reduced HFO synchrony in a pair of tremor cells concurrent with a reduction in firing rate and limb tremor, and decreased HFOs of local field potentials in the STN. These results demonstrate that HFO synchronization in the STN is reduced by voluntary movements and by exogenous dopaminergic medication. A mechanism for neuronal oscillatory synchronization in basal ganglia is proposed. It is suggested that the firing of STN neurones can be synchronized by 15-30 Hz cortical beta oscillatory activity, particularly when dopamine deficiency results in a higher background firing rate of STN neurones, and that this synchronization contributes to parkinsonian pathophysiology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>Ron</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Physiology, University of Toronto, Toronto, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ashby</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Hutchison</LastName><ForeName>William D</ForeName><Initials>WD</Initials></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials></Author><Author ValidYN="Y"><LastName>Lozano</LastName><ForeName>Andres M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Dostrovsky</LastName><ForeName>Jonathan O</ForeName><Initials>JO</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS 40872</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Brain. 2002 Jun;125(Pt 6):1175-6</RefSource><PMID Version="1">12023308</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001683" MajorTopicYN="N">Biological Clocks</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="N">Dopamine Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016343" MajorTopicYN="N">Monitoring, Intraoperative</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>5</Month><Day>23</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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