Subthalamic high frequency stimulation resets subthalamic firing and reduces abnormal oscillations.
Identifieur interne : 000F28 ( PubMed/Corpus ); précédent : 000F27; suivant : 000F29Subthalamic high frequency stimulation resets subthalamic firing and reduces abnormal oscillations.
Auteurs : Wassilios Meissner ; Arthur Leblois ; David Hansel ; Bernard Bioulac ; Christian E. Gross ; Abdelhamid Benazzouz ; Thomas BoraudSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : gamma-Aminobutyric Acid.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurotoxins.
- methods : Electric Stimulation.
- physiology : Action Potentials, Neurons, Subthalamic Nucleus.
- physiopathology : Parkinson Disease.
- Animals, Female, Macaca mulatta.
Abstract
High frequency stimulation (HFS) of the subthalamic nucleus (STN) is a well-established therapeutic approach for the treatment of late-stage Parkinson's disease. Although the underlying cause of this illness remains a mystery, changes in firing rate and synchronized activity in different basal ganglia nuclei have been related to its symptoms. Here we investigated the impact of STN-HFS on firing rate as well as correlated and oscillatory activity in the STN network in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned non-human primates by using simultaneous extracellular single-unit recordings. STN-HFS reduced (i) the firing rate of STN neurons, (ii) the oscillatory activity at an individual STN neuron level as well as (iii) the correlated and oscillatory activity between pairs of STN neurons, while contralateral rigidity was improved. A detailed analysis showed that the decrease of mean firing rate resulted from the resetting of firing probability to virtually zero by the stimulus pulse. Subsequently, STN neurons resumed their activity after a mean duration of 2.9 +/- 0.1 ms and their firing probability returned to baseline values approximately 7 ms after the onset of the stimulus pulse, the recovery of the firing probability being represented by a sigmoid function. Thus, the overall decrease of the mean firing rate resulted from the repetition of this dynamical process with a frequency of 130 Hz (interstimulus interval approximately 7.7 ms), allowing the neuron to fire with its baseline firing rate only for a very short period. Although the mechanisms underlying the desynchronization of neuronal activity in the STN network remain unclear, the resetting of STN neuron firing probability by the electrical stimulus would rather be expected to increase oscillatory activity at an individual neuron level as well as correlated and oscillatory activity between pairs of STN neurons. However, assuming the resetting of firing rate to be the consequence of a transient GABAergic inhibition through excitation of presynaptic GABAergic axon terminals, different recovery periods of STN neurons might delay the appearance of synchronized oscillations, particularly if they are not generated locally. In conclusion, our study provides new evidence that STN-HFS decreases oscillatory activity in the STN network. Although the exact relation between oscillatory activity and Parkinson's disease symptoms remains to be determined, the present results suggest that STN-HFS might at least partially exert its beneficial effects through the reduction of oscillatory activity in the STN network and consequently in the entire cortex-basal ganglia-cortex network.
DOI: 10.1093/brain/awh616
PubMed: 16123144
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pubmed:16123144Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Subthalamic high frequency stimulation resets subthalamic firing and reduces abnormal oscillations.</title><author><name sortKey="Meissner, Wassilios" sort="Meissner, Wassilios" uniqKey="Meissner W" first="Wassilios" last="Meissner">Wassilios Meissner</name><affiliation><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Ségalen, Bordeaux, France. wassilios.meissner@umr5543.u-bordeaux2.fr</nlm:affiliation></affiliation></author><author><name sortKey="Leblois, Arthur" sort="Leblois, Arthur" uniqKey="Leblois A" first="Arthur" last="Leblois">Arthur Leblois</name></author><author><name sortKey="Hansel, David" sort="Hansel, David" uniqKey="Hansel D" first="David" last="Hansel">David Hansel</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="Benazzouz, Abdelhamid" sort="Benazzouz, Abdelhamid" uniqKey="Benazzouz A" first="Abdelhamid" last="Benazzouz">Abdelhamid Benazzouz</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="2005">2005</date><idno type="RBID">pubmed:16123144</idno><idno type="pmid">16123144</idno><idno type="doi">10.1093/brain/awh616</idno><idno type="wicri:Area/PubMed/Corpus">000F28</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F28</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Subthalamic high frequency stimulation resets subthalamic firing and reduces abnormal oscillations.</title><author><name sortKey="Meissner, Wassilios" sort="Meissner, Wassilios" uniqKey="Meissner W" first="Wassilios" last="Meissner">Wassilios Meissner</name><affiliation><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Ségalen, Bordeaux, France. wassilios.meissner@umr5543.u-bordeaux2.fr</nlm:affiliation></affiliation></author><author><name sortKey="Leblois, Arthur" sort="Leblois, Arthur" uniqKey="Leblois A" first="Arthur" last="Leblois">Arthur Leblois</name></author><author><name sortKey="Hansel, David" sort="Hansel, David" uniqKey="Hansel D" first="David" last="Hansel">David Hansel</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="Benazzouz, Abdelhamid" sort="Benazzouz, Abdelhamid" uniqKey="Benazzouz A" first="Abdelhamid" last="Benazzouz">Abdelhamid Benazzouz</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">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2005" type="published">2005</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>Action Potentials (physiology)</term><term>Animals</term><term>Electric Stimulation (methods)</term><term>Female</term><term>Macaca mulatta</term><term>Neurons (physiology)</term><term>Neurotoxins</term><term>Parkinson Disease (physiopathology)</term><term>Subthalamic Nucleus (physiology)</term><term>gamma-Aminobutyric Acid (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Neurotoxins</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</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" xml:lang="en"><term>Animals</term><term>Female</term><term>Macaca mulatta</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High frequency stimulation (HFS) of the subthalamic nucleus (STN) is a well-established therapeutic approach for the treatment of late-stage Parkinson's disease. Although the underlying cause of this illness remains a mystery, changes in firing rate and synchronized activity in different basal ganglia nuclei have been related to its symptoms. Here we investigated the impact of STN-HFS on firing rate as well as correlated and oscillatory activity in the STN network in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned non-human primates by using simultaneous extracellular single-unit recordings. STN-HFS reduced (i) the firing rate of STN neurons, (ii) the oscillatory activity at an individual STN neuron level as well as (iii) the correlated and oscillatory activity between pairs of STN neurons, while contralateral rigidity was improved. A detailed analysis showed that the decrease of mean firing rate resulted from the resetting of firing probability to virtually zero by the stimulus pulse. Subsequently, STN neurons resumed their activity after a mean duration of 2.9 +/- 0.1 ms and their firing probability returned to baseline values approximately 7 ms after the onset of the stimulus pulse, the recovery of the firing probability being represented by a sigmoid function. Thus, the overall decrease of the mean firing rate resulted from the repetition of this dynamical process with a frequency of 130 Hz (interstimulus interval approximately 7.7 ms), allowing the neuron to fire with its baseline firing rate only for a very short period. Although the mechanisms underlying the desynchronization of neuronal activity in the STN network remain unclear, the resetting of STN neuron firing probability by the electrical stimulus would rather be expected to increase oscillatory activity at an individual neuron level as well as correlated and oscillatory activity between pairs of STN neurons. However, assuming the resetting of firing rate to be the consequence of a transient GABAergic inhibition through excitation of presynaptic GABAergic axon terminals, different recovery periods of STN neurons might delay the appearance of synchronized oscillations, particularly if they are not generated locally. In conclusion, our study provides new evidence that STN-HFS decreases oscillatory activity in the STN network. Although the exact relation between oscillatory activity and Parkinson's disease symptoms remains to be determined, the present results suggest that STN-HFS might at least partially exert its beneficial effects through the reduction of oscillatory activity in the STN network and consequently in the entire cortex-basal ganglia-cortex network.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16123144</PMID><DateCreated><Year>2005</Year><Month>09</Month><Day>26</Day></DateCreated><DateCompleted><Year>2005</Year><Month>12</Month><Day>29</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>128</Volume><Issue>Pt 10</Issue><PubDate><Year>2005</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Subthalamic high frequency stimulation resets subthalamic firing and reduces abnormal oscillations.</ArticleTitle><Pagination><MedlinePgn>2372-82</MedlinePgn></Pagination><Abstract><AbstractText>High frequency stimulation (HFS) of the subthalamic nucleus (STN) is a well-established therapeutic approach for the treatment of late-stage Parkinson's disease. Although the underlying cause of this illness remains a mystery, changes in firing rate and synchronized activity in different basal ganglia nuclei have been related to its symptoms. Here we investigated the impact of STN-HFS on firing rate as well as correlated and oscillatory activity in the STN network in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned non-human primates by using simultaneous extracellular single-unit recordings. STN-HFS reduced (i) the firing rate of STN neurons, (ii) the oscillatory activity at an individual STN neuron level as well as (iii) the correlated and oscillatory activity between pairs of STN neurons, while contralateral rigidity was improved. A detailed analysis showed that the decrease of mean firing rate resulted from the resetting of firing probability to virtually zero by the stimulus pulse. Subsequently, STN neurons resumed their activity after a mean duration of 2.9 +/- 0.1 ms and their firing probability returned to baseline values approximately 7 ms after the onset of the stimulus pulse, the recovery of the firing probability being represented by a sigmoid function. Thus, the overall decrease of the mean firing rate resulted from the repetition of this dynamical process with a frequency of 130 Hz (interstimulus interval approximately 7.7 ms), allowing the neuron to fire with its baseline firing rate only for a very short period. Although the mechanisms underlying the desynchronization of neuronal activity in the STN network remain unclear, the resetting of STN neuron firing probability by the electrical stimulus would rather be expected to increase oscillatory activity at an individual neuron level as well as correlated and oscillatory activity between pairs of STN neurons. However, assuming the resetting of firing rate to be the consequence of a transient GABAergic inhibition through excitation of presynaptic GABAergic axon terminals, different recovery periods of STN neurons might delay the appearance of synchronized oscillations, particularly if they are not generated locally. In conclusion, our study provides new evidence that STN-HFS decreases oscillatory activity in the STN network. Although the exact relation between oscillatory activity and Parkinson's disease symptoms remains to be determined, the present results suggest that STN-HFS might at least partially exert its beneficial effects through the reduction of oscillatory activity in the STN network and consequently in the entire cortex-basal ganglia-cortex network.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meissner</LastName><ForeName>Wassilios</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Ségalen, Bordeaux, France. wassilios.meissner@umr5543.u-bordeaux2.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leblois</LastName><ForeName>Arthur</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Hansel</LastName><ForeName>David</ForeName><Initials>D</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>Benazzouz</LastName><ForeName>Abdelhamid</ForeName><Initials>A</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><ArticleDate DateType="Electronic"><Year>2005</Year><Month>08</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>56-12-2</RegistryNumber><NameOfSubstance UI="D005680">gamma-Aminobutyric Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Brain. 2006 Dec;129(Pt 12):e59; author reply e60</RefSource><PMID Version="1">17132638</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008253" MajorTopicYN="N">Macaca mulatta</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009498" MajorTopicYN="N">Neurotoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005680" MajorTopicYN="N">gamma-Aminobutyric Acid</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>8</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>12</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>8</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16123144</ArticleId><ArticleId IdType="pii">awh616</ArticleId><ArticleId IdType="doi">10.1093/brain/awh616</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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