Molecular mechanisms underlying levodopa-induced dyskinesia.
Identifieur interne : 002056 ( PubMed/Curation ); précédent : 002055; suivant : 002057Molecular mechanisms underlying levodopa-induced dyskinesia.
Auteurs : Paolo Calabresi [Italie] ; Massimiliano Di Filippo ; Veronica Ghiglieri ; Barbara PicconiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Antiparkinson Agents (adverse effects), Dopamine and cAMP-Regulated Phosphoprotein 32 (drug effects), Dopamine and cAMP-Regulated Phosphoprotein 32 (physiology), Humans, Levodopa (adverse effects), Movement Disorders (etiology), Neuronal Plasticity (drug effects), Neuronal Plasticity (physiology), Receptors, Dopamine D1 (drug effects), Receptors, Dopamine D1 (physiology), Receptors, Dopamine D2 (drug effects), Receptors, Dopamine D2 (physiology).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , drug effects : Dopamine and cAMP-Regulated Phosphoprotein 32, Receptors, Dopamine D1, Receptors, Dopamine D2.
- chemical , physiology : Dopamine and cAMP-Regulated Phosphoprotein 32, Receptors, Dopamine D1, Receptors, Dopamine D2.
- drug effects : Neuronal Plasticity.
- etiology : Movement Disorders.
- physiology : Neuronal Plasticity.
- Humans.
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 D1 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.
DOI: 10.1002/mds.22019
PubMed: 18781674
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Maria della Misericordia, Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Di Filippo, Massimiliano" sort="Di Filippo, Massimiliano" uniqKey="Di Filippo M" first="Massimiliano" last="Di Filippo">Massimiliano Di Filippo</name></author><author><name sortKey="Ghiglieri, Veronica" sort="Ghiglieri, Veronica" uniqKey="Ghiglieri V" first="Veronica" last="Ghiglieri">Veronica Ghiglieri</name></author><author><name sortKey="Picconi, Barbara" sort="Picconi, Barbara" uniqKey="Picconi B" first="Barbara" last="Picconi">Barbara Picconi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22019</idno><idno type="RBID">pubmed:18781674</idno><idno type="pmid">18781674</idno><idno type="wicri:Area/PubMed/Corpus">002056</idno><idno type="wicri:Area/PubMed/Curation">002056</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Molecular mechanisms underlying levodopa-induced dyskinesia.</title><author><name sortKey="Calabresi, Paolo" sort="Calabresi, Paolo" uniqKey="Calabresi P" first="Paolo" last="Calabresi">Paolo Calabresi</name><affiliation wicri:level="1"><nlm:affiliation>Clinica Neurologica, Università degli Studi di Perugia, Ospedale S. 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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 D1 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><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18781674</PMID><DateCreated><Year>2008</Year><Month>09</Month><Day>18</Day></DateCreated><DateCompleted><Year>2009</Year><Month>02</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23 Suppl 3</Volume><PubDate><Year>2008</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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In particular, we will address the role of both DA D1 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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