Molecular Mechanisms Underlying Levodopa-Induced Dyskinesia
Identifieur interne : 001190 ( PascalFrancis/Checkpoint ); précédent : 001189; suivant : 001191Molecular Mechanisms Underlying Levodopa-Induced Dyskinesia
Auteurs : Paolo Calabresi [Italie] ; Massimiliano Di Filippo [Italie] ; Veronica Ghiglieri [Italie] ; Barbara Picconi [Italie]Source :
- Movement disorders [ 0885-3185 ] ; 2008.
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- Pascal (Inist)
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Abstract
Although levodopa remains the most effective drug for the symptomatic treatment of Parkinson's disease, chronic therapy with this pharmacological compound initiates a complex cascade of cellular and molecular downstream effects resulting in the development of abnormal involuntary movements. The precise mechanisms underlying the development of levodopa induced dyskinesia, however, are far from being completely elucidated. In the present review, we will describe changes in long-term synaptic excitability following dopamine (DA) denervation and long-term levodopa treatment leading to abnormal involuntary movements. In particular, we will address the role of both DA Dl receptors and NMDA glutamate receptors in the induction and maintenance of dyskinesia and abnormal synaptic plasticity. We will also describe the possible interaction between these two receptors in the pathophysiology of dyskinesia taking the advantage of the existing knowledge concerning the mechanisms underlying drug abuse. This latter pathophysiological condition, in fact, seems to share several biochemical transduction pathways with those implicated in levodopa-induced dyskinesia. Finally, we will briefly discuss the possible implication of A2A adenosine receptors in long-term motor complications of levodopa therapy and focus on the interaction between A2A and D2 receptors. Future studies are required to understand how the interaction between these various biochemical steps converge to produce a long-term change in neuronal excitability within the basal ganglia leading to abnormal involuntary movements following levodopa treatment in the DA-denervated state.
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Maria della Misericordia</s1><s2>Perugia</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Italie</country><wicri:noRegion>Perugia</wicri:noRegion></affiliation><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>IRCCS Fondazione Santa Lucia</s1><s2>Rome</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Italie</country><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Ghiglieri, Veronica" sort="Ghiglieri, Veronica" uniqKey="Ghiglieri V" first="Veronica" last="Ghiglieri">Veronica Ghiglieri</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>IRCCS Fondazione Santa Lucia</s1><s2>Rome</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Italie</country><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Picconi, Barbara" sort="Picconi, Barbara" uniqKey="Picconi B" first="Barbara" last="Picconi">Barbara Picconi</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>IRCCS Fondazione Santa Lucia</s1><s2>Rome</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Italie</country><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></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="2008">2008</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>Parkinson disease</term><term>Synaptic plasticity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dyskinésie</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Lévodopa</term><term>Plasticité synaptique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although levodopa remains the most effective drug for the symptomatic treatment of Parkinson's disease, chronic therapy with this pharmacological compound initiates a complex cascade of cellular and molecular downstream effects resulting in the development of abnormal involuntary movements. The precise mechanisms underlying the development of levodopa induced dyskinesia, however, are far from being completely elucidated. In the present review, we will describe changes in long-term synaptic excitability following dopamine (DA) denervation and long-term levodopa treatment leading to abnormal involuntary movements. In particular, we will address the role of both DA Dl receptors and NMDA glutamate receptors in the induction and maintenance of dyskinesia and abnormal synaptic plasticity. We will also describe the possible interaction between these two receptors in the pathophysiology of dyskinesia taking the advantage of the existing knowledge concerning the mechanisms underlying drug abuse. This latter pathophysiological condition, in fact, seems to share several biochemical transduction pathways with those implicated in levodopa-induced dyskinesia. Finally, we will briefly discuss the possible implication of A2A adenosine receptors in long-term motor complications of levodopa therapy and focus on the interaction between A2A and D2 receptors. Future studies are required to understand how the interaction between these various biochemical steps converge to produce a long-term change in neuronal excitability within the basal ganglia leading to abnormal involuntary movements following levodopa treatment in the DA-denervated state.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>23</s2></fA05><fA06><s3>SUP3</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Molecular Mechanisms Underlying Levodopa-Induced Dyskinesia</s1></fA08><fA09 i1="01" i2="1" l="ENG"><s1>Levodopa Treatment and Motor Complications in Parkinson's Disease: Scientific Basis and Therapeutic Approaches</s1></fA09><fA11 i1="01" i2="1"><s1>CALABRESI (Paolo)</s1></fA11><fA11 i1="02" i2="1"><s1>DI FILIPPO (Massimiliano)</s1></fA11><fA11 i1="03" i2="1"><s1>GHIGLIERI (Veronica)</s1></fA11><fA11 i1="04" i2="1"><s1>PICCONI (Barbara)</s1></fA11><fA12 i1="01" i2="1"><s1>OLANOW (C. 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In particular, we will address the role of both DA Dl receptors and NMDA glutamate receptors in the induction and maintenance of dyskinesia and abnormal synaptic plasticity. We will also describe the possible interaction between these two receptors in the pathophysiology of dyskinesia taking the advantage of the existing knowledge concerning the mechanisms underlying drug abuse. This latter pathophysiological condition, in fact, seems to share several biochemical transduction pathways with those implicated in levodopa-induced dyskinesia. Finally, we will briefly discuss the possible implication of A2A adenosine receptors in long-term motor complications of levodopa therapy and focus on the interaction between A2A and D2 receptors. 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