Apomorphine reduces subthalamic neuronal entropy in parkinsonian patients.
Identifieur interne : 000C96 ( PubMed/Curation ); précédent : 000C95; suivant : 000C97Apomorphine reduces subthalamic neuronal entropy in parkinsonian patients.
Auteurs : M. Lafreniere-Roula [Canada] ; O. Darbin ; W D Hutchison ; T. Wichmann ; A M Lozano ; J O DostrovskySource :
- Experimental neurology [ 1090-2430 ] ; 2010.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Apomorphine.
- drug effects : Action Potentials, Neurons, Subthalamic Nucleus.
- drug therapy : Parkinson Disease.
- Deep Brain Stimulation, Entropy, Humans.
Abstract
Dopamine depletion in Parkinson's disease (PD) alters the neuronal activity in basal ganglia circuits. Characterizing these changes in network activity is an important step in understanding the disease and how therapies mitigate symptoms. Non-linear analysis methods can complement the traditional description of neuronal firing characteristics. Here we examine the entropy of subthalamic neurons in PD patients undergoing stereotactic surgery for deep brain stimulation (DBS). The activity of 8 neurons was recorded prior to, during, and following systemic administration of the dopamine agonist apomorphine at clinically effective doses. Apomorphine induced a decrease in entropy measured in the inter-spike intervals of sub-thalamic neurons in 6 of the 8 neurons. This is the first report that anti-parkinsonian drugs affect non-linear features of neuronal firing in the basal ganglia of parkinsonian patients.
DOI: 10.1016/j.expneurol.2010.07.016
PubMed: 20659454
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Darbin</name></author><author><name sortKey="Hutchison, W D" sort="Hutchison, W D" uniqKey="Hutchison W" first="W D" last="Hutchison">W D Hutchison</name></author><author><name sortKey="Wichmann, T" sort="Wichmann, T" uniqKey="Wichmann T" first="T" last="Wichmann">T. Wichmann</name></author><author><name sortKey="Lozano, A M" sort="Lozano, A M" uniqKey="Lozano A" first="A M" last="Lozano">A M Lozano</name></author><author><name sortKey="Dostrovsky, J O" sort="Dostrovsky, J O" uniqKey="Dostrovsky J" first="J O" last="Dostrovsky">J O Dostrovsky</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20659454</idno><idno type="pmid">20659454</idno><idno type="doi">10.1016/j.expneurol.2010.07.016</idno><idno type="wicri:Area/PubMed/Corpus">000C96</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000C96</idno><idno type="wicri:Area/PubMed/Curation">000C96</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000C96</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Apomorphine reduces subthalamic neuronal entropy in parkinsonian patients.</title><author><name sortKey="Lafreniere Roula, M" sort="Lafreniere Roula, M" uniqKey="Lafreniere Roula M" first="M" last="Lafreniere-Roula">M. Lafreniere-Roula</name><affiliation wicri:level="1"><nlm:affiliation>Department of Physiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. myriam.lafreniere.roula@utoronto.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Physiology, University of Toronto, Toronto, ON, M5S 1A8</wicri:regionArea></affiliation></author><author><name sortKey="Darbin, O" sort="Darbin, O" uniqKey="Darbin O" first="O" last="Darbin">O. Darbin</name></author><author><name sortKey="Hutchison, W D" sort="Hutchison, W D" uniqKey="Hutchison W" first="W D" last="Hutchison">W D Hutchison</name></author><author><name sortKey="Wichmann, T" sort="Wichmann, T" uniqKey="Wichmann T" first="T" last="Wichmann">T. Wichmann</name></author><author><name sortKey="Lozano, A M" sort="Lozano, A M" uniqKey="Lozano A" first="A M" last="Lozano">A M Lozano</name></author><author><name sortKey="Dostrovsky, J O" sort="Dostrovsky, J O" uniqKey="Dostrovsky J" first="J O" last="Dostrovsky">J O Dostrovsky</name></author></analytic><series><title level="j">Experimental neurology</title><idno type="eISSN">1090-2430</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (drug effects)</term><term>Apomorphine (therapeutic use)</term><term>Deep Brain Stimulation</term><term>Entropy</term><term>Humans</term><term>Neurons (drug effects)</term><term>Parkinson Disease (drug therapy)</term><term>Subthalamic Nucleus (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</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" xml:lang="en"><term>Deep Brain Stimulation</term><term>Entropy</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopamine depletion in Parkinson's disease (PD) alters the neuronal activity in basal ganglia circuits. Characterizing these changes in network activity is an important step in understanding the disease and how therapies mitigate symptoms. Non-linear analysis methods can complement the traditional description of neuronal firing characteristics. Here we examine the entropy of subthalamic neurons in PD patients undergoing stereotactic surgery for deep brain stimulation (DBS). The activity of 8 neurons was recorded prior to, during, and following systemic administration of the dopamine agonist apomorphine at clinically effective doses. Apomorphine induced a decrease in entropy measured in the inter-spike intervals of sub-thalamic neurons in 6 of the 8 neurons. This is the first report that anti-parkinsonian drugs affect non-linear features of neuronal firing in the basal ganglia of parkinsonian patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20659454</PMID><DateCreated><Year>2010</Year><Month>09</Month><Day>13</Day></DateCreated><DateCompleted><Year>2010</Year><Month>10</Month><Day>01</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2430</ISSN><JournalIssue CitedMedium="Internet"><Volume>225</Volume><Issue>2</Issue><PubDate><Year>2010</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Experimental neurology</Title><ISOAbbreviation>Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Apomorphine reduces subthalamic neuronal entropy in parkinsonian patients.</ArticleTitle><Pagination><MedlinePgn>455-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.expneurol.2010.07.016</ELocationID><Abstract><AbstractText>Dopamine depletion in Parkinson's disease (PD) alters the neuronal activity in basal ganglia circuits. Characterizing these changes in network activity is an important step in understanding the disease and how therapies mitigate symptoms. Non-linear analysis methods can complement the traditional description of neuronal firing characteristics. Here we examine the entropy of subthalamic neurons in PD patients undergoing stereotactic surgery for deep brain stimulation (DBS). The activity of 8 neurons was recorded prior to, during, and following systemic administration of the dopamine agonist apomorphine at clinically effective doses. Apomorphine induced a decrease in entropy measured in the inter-spike intervals of sub-thalamic neurons in 6 of the 8 neurons. This is the first report that anti-parkinsonian drugs affect non-linear features of neuronal firing in the basal ganglia of parkinsonian patients.</AbstractText><CopyrightInformation>Copyright © 2010 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lafreniere-Roula</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Physiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. myriam.lafreniere.roula@utoronto.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Darbin</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Hutchison</LastName><ForeName>W D</ForeName><Initials>WD</Initials></Author><Author ValidYN="Y"><LastName>Wichmann</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Lozano</LastName><ForeName>A M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Dostrovsky</LastName><ForeName>J O</ForeName><Initials>JO</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS054976</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-NS054976</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51 RR000165</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>MOP 42505</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>RR-000165</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>07</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Exp Neurol</MedlineTA><NlmUniqueID>0370712</NlmUniqueID><ISSNLinking>0014-4886</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>N21FAR7B4S</RegistryNumber><NameOfSubstance UI="D001058">Apomorphine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol. 1994 Apr;266(4 Pt 2):H1643-56</RefSource><PMID Version="1">8184944</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2006 Nov 6;1118(1):84-93</RefSource><PMID Version="1">16989784</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Chaos. 1995 Mar;5(1):110-117</RefSource><PMID Version="1">12780163</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 1995 Feb;18(2):63-4</RefSource><PMID Version="1">7537410</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 1996 Jun;72(3):863-76</RefSource><PMID Version="1">9157332</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Brain Res. 2003 Jul;151(2):167-72</RefSource><PMID Version="1">12768261</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Obstet Gynecol. 1998 Aug;10(4):281-91</RefSource><PMID Version="1">9719878</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Epilepsia. 2002 Apr;43(4):336-41</RefSource><PMID Version="1">11952762</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2000 Jun;278(6):H2039-49</RefSource><PMID Version="1">10843903</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1997 Sep 1;17(17):6807-19</RefSource><PMID Version="1">9254691</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Theor Biol. 1996 Nov 21;183(2):219-30</RefSource><PMID Version="1">8977879</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Epilepsia. 2003 Jul;44(7):912-6</RefSource><PMID Version="1">12823573</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2009 Dec;15 Suppl 3:S156-61</RefSource><PMID Version="1">20082980</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurophysiol. 2001 Jul;86(1):249-60</RefSource><PMID Version="1">11431506</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci Methods. 1996 Oct;68(2):211-23</RefSource><PMID Version="1">8912194</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2000 Oct;38(1):38-50</RefSource><PMID Version="1">10941139</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosurgery. 2007 Apr;60(4 Suppl 2):277-83; 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