Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment
Identifieur interne : 000C24 ( PascalFrancis/Checkpoint ); précédent : 000C23; suivant : 000C25Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment
Auteurs : Pauline Belujon [États-Unis] ; Daniel J. Lodge [États-Unis] ; Anthony A. Grace [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2010.
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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.
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Grace</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Departments of Neuroscience, Psychiatry, and Psychology, University of Pittsburgh</s1><s2>Pittsburgh, PA</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dyskinesia</term><term>Levodopa</term><term>Nervous system diseases</term><term>Plasticity</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dyskinésie</term><term>Pathologie du système nerveux</term><term>Plasticité</term><term>Lévodopa</term><term>Traitement</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 <sub>L</sub>-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 <sub>L</sub>-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic <sub>L</sub>-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. 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All rights reserved.</s1></fA44><fA45><s0>38 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0413274</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as <sub>L</sub>-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 <sub>L</sub>-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic <sub>L</sub>-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. 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Grace</name><name sortKey="Lodge, Daniel J" sort="Lodge, Daniel J" uniqKey="Lodge D" first="Daniel J." last="Lodge">Daniel J. Lodge</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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