High-frequency stimulation of the subthalamic nucleus potentiates L-DOPA-induced neurochemical changes in the striatum in a rat model of Parkinson's disease.
Identifieur interne : 000D63 ( PubMed/Curation ); précédent : 000D62; suivant : 000D64High-frequency stimulation of the subthalamic nucleus potentiates L-DOPA-induced neurochemical changes in the striatum in a rat model of Parkinson's disease.
Auteurs : Abid Oueslati [France] ; Véronique Sgambato-Faure ; Christophe Melon ; Philippe Kachidian ; Paolo Gubellini ; Mohammed Amri ; Lydia Kerkerian-Le Goff ; Pascal SalinSource :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 1529-2401 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Biomarkers (metabolism), Deep Brain Stimulation, Denervation, Disease Models, Animal, Drug Synergism, Dyskinesias (drug therapy), Dyskinesias (etiology), Dyskinesias (physiopathology), Electron Transport Complex IV (metabolism), Levodopa (pharmacology), Male, Motor Cortex (physiopathology), Neuropeptides (metabolism), Parkinson Disease (complications), Parkinson Disease (physiopathology), Proto-Oncogene Proteins c-fos (metabolism), Rats, Rats, Wistar, Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , metabolism : Biomarkers, Electron Transport Complex IV, Neuropeptides, Proto-Oncogene Proteins c-fos.
- complications : Parkinson Disease.
- drug therapy : Dyskinesias.
- etiology : Dyskinesias.
- chemical , pharmacology : Levodopa.
- physiopathology : Dyskinesias, Motor Cortex, Parkinson Disease, Subthalamic Nucleus.
- Animals, Deep Brain Stimulation, Denervation, Disease Models, Animal, Drug Synergism, Male, Rats, Rats, Wistar.
Abstract
This study examined the cellular changes produced in the striatum by chronic L-DOPA treatment and prolonged subthalamic nucleus high-frequency stimulation (STN-HFS) applied separately, successively, or in association, in the 6-hydroxydopamine-lesioned rat model of Parkinson's disease (PD). Only animals showing severe L-DOPA-induced dyskinesias (LIDs) were included, and STN-HFS was applied for 5 d at an intensity efficient for alleviating akinesia without inducing dyskinesias. L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. STN-HFS did not affect per se the postlesion changes in any of these markers. However, when applied in association with L-DOPA treatment, it potentiated the positive modulation exerted by L-DOPA on all of the markers examined and tended to exacerbate LIDs. After 5 d of L-DOPA withdrawal, the only persisting drug-induced responses were an elevation in preprodynorphin mRNA levels and in the number of FosB/deltaFosB-immunoreactive neurons. Selective additional increases in these two markers were measured when STN-HFS was applied subsequently to L-DOPA treatment. These data provide the first evidence that STN-HFS exacerbates the responsiveness of striatal cells to L-DOPA medication and suggest that STN-HFS acts specifically through an L-DOPA-modulated signal transduction pathway associated with LIDs in the striatum. They point to striatal cells as a primary site for the complex interactions between these two therapeutic approaches in PD and argue against a direct anti-dyskinetic action of STN-HFS.
DOI: 10.1523/JNEUROSCI.2949-06.2007
PubMed: 17329435
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Institute of Marseille Luminy, Unité Mixte de Recherche 6216, Centre National de la Recherche Scientifique-Université de la Méditerranée, 13402 Marseille cedex 20, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Developmental Biology Institute of Marseille Luminy, Unité Mixte de Recherche 6216, Centre National de la Recherche Scientifique-Université de la Méditerranée, 13402 Marseille cedex 20</wicri:regionArea></affiliation></author><author><name sortKey="Sgambato Faure, Veronique" sort="Sgambato Faure, Veronique" uniqKey="Sgambato Faure V" first="Véronique" last="Sgambato-Faure">Véronique Sgambato-Faure</name></author><author><name sortKey="Melon, Christophe" sort="Melon, Christophe" uniqKey="Melon C" first="Christophe" last="Melon">Christophe Melon</name></author><author><name sortKey="Kachidian, Philippe" sort="Kachidian, Philippe" uniqKey="Kachidian P" first="Philippe" last="Kachidian">Philippe Kachidian</name></author><author><name sortKey="Gubellini, Paolo" sort="Gubellini, Paolo" uniqKey="Gubellini P" first="Paolo" last="Gubellini">Paolo Gubellini</name></author><author><name sortKey="Amri, Mohammed" sort="Amri, Mohammed" uniqKey="Amri M" first="Mohammed" last="Amri">Mohammed Amri</name></author><author><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></author></analytic><series><title level="j">The Journal of neuroscience : the official journal of the Society for Neuroscience</title><idno type="eISSN">1529-2401</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biomarkers (metabolism)</term><term>Deep Brain Stimulation</term><term>Denervation</term><term>Disease Models, Animal</term><term>Drug Synergism</term><term>Dyskinesias (drug therapy)</term><term>Dyskinesias (etiology)</term><term>Dyskinesias (physiopathology)</term><term>Electron Transport Complex IV (metabolism)</term><term>Levodopa (pharmacology)</term><term>Male</term><term>Motor Cortex (physiopathology)</term><term>Neuropeptides (metabolism)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (physiopathology)</term><term>Proto-Oncogene Proteins c-fos (metabolism)</term><term>Rats</term><term>Rats, Wistar</term><term>Subthalamic Nucleus (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>Electron Transport Complex IV</term><term>Neuropeptides</term><term>Proto-Oncogene Proteins c-fos</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesias</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesias</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesias</term><term>Motor Cortex</term><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Deep Brain Stimulation</term><term>Denervation</term><term>Disease Models, Animal</term><term>Drug Synergism</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study examined the cellular changes produced in the striatum by chronic L-DOPA treatment and prolonged subthalamic nucleus high-frequency stimulation (STN-HFS) applied separately, successively, or in association, in the 6-hydroxydopamine-lesioned rat model of Parkinson's disease (PD). Only animals showing severe L-DOPA-induced dyskinesias (LIDs) were included, and STN-HFS was applied for 5 d at an intensity efficient for alleviating akinesia without inducing dyskinesias. L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. STN-HFS did not affect per se the postlesion changes in any of these markers. However, when applied in association with L-DOPA treatment, it potentiated the positive modulation exerted by L-DOPA on all of the markers examined and tended to exacerbate LIDs. After 5 d of L-DOPA withdrawal, the only persisting drug-induced responses were an elevation in preprodynorphin mRNA levels and in the number of FosB/deltaFosB-immunoreactive neurons. Selective additional increases in these two markers were measured when STN-HFS was applied subsequently to L-DOPA treatment. These data provide the first evidence that STN-HFS exacerbates the responsiveness of striatal cells to L-DOPA medication and suggest that STN-HFS acts specifically through an L-DOPA-modulated signal transduction pathway associated with LIDs in the striatum. They point to striatal cells as a primary site for the complex interactions between these two therapeutic approaches in PD and argue against a direct anti-dyskinetic action of STN-HFS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17329435</PMID><DateCreated><Year>2007</Year><Month>03</Month><Day>01</Day></DateCreated><DateCompleted><Year>2007</Year><Month>03</Month><Day>19</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1529-2401</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>9</Issue><PubDate><Year>2007</Year><Month>Feb</Month><Day>28</Day></PubDate></JournalIssue><Title>The Journal of neuroscience : the official journal of the Society for Neuroscience</Title><ISOAbbreviation>J. 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L-DOPA treatment alone induced FosB/deltaFosB immunoreactivity, exacerbated the postlesional increase in preproenkephalin, reversed the decrease in preprotachykinin, and markedly increased mRNA levels of preprodynorphin and of the glial glutamate transporter GLT1, which were respectively decreased and unaffected by the dopamine lesion. STN-HFS did not affect per se the postlesion changes in any of these markers. However, when applied in association with L-DOPA treatment, it potentiated the positive modulation exerted by L-DOPA on all of the markers examined and tended to exacerbate LIDs. After 5 d of L-DOPA withdrawal, the only persisting drug-induced responses were an elevation in preprodynorphin mRNA levels and in the number of FosB/deltaFosB-immunoreactive neurons. Selective additional increases in these two markers were measured when STN-HFS was applied subsequently to L-DOPA treatment. These data provide the first evidence that STN-HFS exacerbates the responsiveness of striatal cells to L-DOPA medication and suggest that STN-HFS acts specifically through an L-DOPA-modulated signal transduction pathway associated with LIDs in the striatum. 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