Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment.
Identifieur interne : 001764 ( PubMed/Corpus ); précédent : 001763; suivant : 001765Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment.
Auteurs : Pauline Belujon ; Daniel J. Lodge ; Anthony A. GraceSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Action Potentials (drug effects), Action Potentials (physiology), Animals, Antiparkinson Agents (adverse effects), Behavior, Animal (drug effects), Cholera Toxin (metabolism), Corpus Striatum (cytology), Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Disease Models, Animal, Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (pathology), Dyskinesia, Drug-Induced (physiopathology), Fluorescent Dyes (metabolism), Levodopa (adverse effects), Long-Term Potentiation (drug effects), Long-Term Potentiation (physiology), Neuronal Plasticity (drug effects), Neuronal Plasticity (physiology), Neurons (drug effects), Neurons (metabolism), Neurons (pathology), Neurons (physiology), Oxidopamine (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Rats, Substantia Nigra (drug effects), Substantia Nigra (physiopathology), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- cytology : Corpus Striatum.
- drug effects : Action Potentials, Behavior, Animal, Corpus Striatum, Long-Term Potentiation, Neuronal Plasticity, Neurons, Substantia Nigra.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced, Parkinson Disease.
- chemical , metabolism : Cholera Toxin, Fluorescent Dyes, Neurons, Tyrosine 3-Monooxygenase.
- pathology : Dyskinesia, Drug-Induced, Neurons.
- physiology : Action Potentials, Long-Term Potentiation, Neuronal Plasticity, Neurons.
- physiopathology : Corpus Striatum, Dyskinesia, Drug-Induced, Substantia Nigra.
- chemical , toxicity : Oxidopamine.
- Animals, Disease Models, Animal, Rats.
Abstract
Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.
DOI: 10.1002/mds.23245
PubMed: 20623773
Links to Exploration step
pubmed:20623773Le document en format XML
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Grace</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23245</idno><idno type="RBID">pubmed:20623773</idno><idno type="pmid">20623773</idno><idno type="wicri:Area/PubMed/Corpus">001764</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment.</title><author><name sortKey="Belujon, Pauline" sort="Belujon, Pauline" uniqKey="Belujon P" first="Pauline" last="Belujon">Pauline Belujon</name><affiliation><nlm:affiliation>Departments of Neuroscience, Psychiatry, and Psychology, University of Pittsburgh, Pittsburgh, PA 15260, USA. belujon@pitt.edu</nlm:affiliation></affiliation></author><author><name sortKey="Lodge, Daniel J" sort="Lodge, Daniel J" uniqKey="Lodge D" first="Daniel J" last="Lodge">Daniel J. 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Grace</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</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>Action Potentials (physiology)</term><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Behavior, Animal (drug effects)</term><term>Cholera Toxin (metabolism)</term><term>Corpus Striatum (cytology)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (physiopathology)</term><term>Disease Models, Animal</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (pathology)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Fluorescent Dyes (metabolism)</term><term>Levodopa (adverse effects)</term><term>Long-Term Potentiation (drug effects)</term><term>Long-Term Potentiation (physiology)</term><term>Neuronal Plasticity (drug effects)</term><term>Neuronal Plasticity (physiology)</term><term>Neurons (drug effects)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Neurons (physiology)</term><term>Oxidopamine (toxicity)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (etiology)</term><term>Rats</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (physiopathology)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</term><term>Behavior, Animal</term><term>Corpus Striatum</term><term>Long-Term Potentiation</term><term>Neuronal Plasticity</term><term>Neurons</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cholera Toxin</term><term>Fluorescent Dyes</term><term>Neurons</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Long-Term Potentiation</term><term>Neuronal Plasticity</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Dyskinesia, Drug-Induced</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20623773</PMID><DateCreated><Year>2010</Year><Month>08</Month><Day>26</Day></DateCreated><DateCompleted><Year>2010</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>11</Issue><PubDate><Year>2010</Year><Month>Aug</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment.</ArticleTitle><Pagination><MedlinePgn>1568-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23245</ELocationID><Abstract><AbstractText>Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Belujon</LastName><ForeName>Pauline</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Departments of Neuroscience, Psychiatry, and Psychology, University of Pittsburgh, Pittsburgh, PA 15260, USA. belujon@pitt.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lodge</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Grace</LastName><ForeName>Anthony A</ForeName><Initials>AA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>DA15408</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>MH57440</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 MH057440</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 MH057440-15</GrantID><Acronym>MH</Acronym><Agency>NIMH 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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005456">Fluorescent Dyes</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9012-63-9</RegistryNumber><NameOfSubstance UI="D002772">Cholera Toxin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):7036-40</RefSource><PMID Version="1">9192687</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1997 Jun 15;17(12):4536-44</RefSource><PMID Version="1">9169514</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 1999;14 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UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016627">Oxidopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000633">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" 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