Distinct Changes in cAMP and Extracellular Signal-Regulated Protein Kinase Signalling in L-DOPA-Induced Dyskinesia
Identifieur interne : 000766 ( Pmc/Checkpoint ); précédent : 000765; suivant : 000767Distinct Changes in cAMP and Extracellular Signal-Regulated Protein Kinase Signalling in L-DOPA-Induced Dyskinesia
Auteurs : Emanuela Santini [Suède] ; Veronique Sgambato-Faure [France] ; Qin Li [France, République populaire de Chine] ; Marc Savasta [France] ; Sandra Dovero [France] ; Gilberto Fisone [Suède] ; Erwan Bezard [France, République populaire de Chine]Source :
- PLoS ONE [ 1932-6203 ] ; 2010.
Abstract
In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. However, very little is known, in non-human primates, about the regulation of these signalling cascades and their association with the induction, manifestation and/or maintenance of dyskinesia.
We here studied, in the gold-standard non-human primate model of Parkinson's disease, the changes in PKA-dependent phosphorylation of DARPP-32 and GluR1 AMPA receptor, as well as in ERK and ribosomal protein S6 (S6) phosphorylation, associated to acute and chronic administration of L-DOPA. Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. In contrast, phosphorylation of ERK and S6 was enhanced preferentially after acute L-DOPA administration and decreased during the course of chronic treatment.
Dysregulation of cAMP signalling is maintained during the course of chronic L-DOPA administration, while abnormal ERK signalling peaks during the initial phase of L-DOPA treatment and decreases following prolonged exposure. While cAMP signalling enhancement is associated with dyskinesia, abnormal ERK signalling is associated with priming.
Url:
DOI: 10.1371/journal.pone.0012322
PubMed: 20808799
PubMed Central: 2925943
Affiliations:
- France, République populaire de Chine, Suède
- Aquitaine, Auvergne-Rhône-Alpes, Nouvelle-Aquitaine, Rhône-Alpes, Svealand
- Bordeaux, Grenoble, Pékin, Stockholm
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PMC:2925943Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. However, very little is known, in non-human primates, about the regulation of these signalling cascades and their association with the induction, manifestation and/or maintenance of dyskinesia.</p>
</sec>
<sec><title>Methodology/Results</title>
<p>We here studied, in the gold-standard non-human primate model of Parkinson's disease, the changes in PKA-dependent phosphorylation of DARPP-32 and GluR1 AMPA receptor, as well as in ERK and ribosomal protein S6 (S6) phosphorylation, associated to acute and chronic administration of L-DOPA. Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. In contrast, phosphorylation of ERK and S6 was enhanced preferentially after acute L-DOPA administration and decreased during the course of chronic treatment.</p>
</sec>
<sec><title>Conclusion</title>
<p>Dysregulation of cAMP signalling is maintained during the course of chronic L-DOPA administration, while abnormal ERK signalling peaks during the initial phase of L-DOPA treatment and decreases following prolonged exposure. While cAMP signalling enhancement is associated with dyskinesia, abnormal ERK signalling is associated with priming.</p>
</sec>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id>
<journal-id journal-id-type="publisher-id">plos</journal-id>
<journal-id journal-id-type="pmc">plosone</journal-id>
<journal-title-group><journal-title>PLoS ONE</journal-title>
</journal-title-group>
<issn pub-type="epub">1932-6203</issn>
<publisher><publisher-name>Public Library of Science</publisher-name>
<publisher-loc>San Francisco, USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">20808799</article-id>
<article-id pub-id-type="pmc">2925943</article-id>
<article-id pub-id-type="publisher-id">10-PONE-RA-20049R1</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0012322</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
<subj-group subj-group-type="Discipline"><subject>Neuroscience/Neurobiology of Disease and Regeneration</subject>
<subject>Neuroscience/Neuronal Signaling Mechanisms</subject>
<subject>Neurological Disorders/Movement Disorders</subject>
</subj-group>
</article-categories>
<title-group><article-title>Distinct Changes in cAMP and Extracellular Signal-Regulated Protein Kinase Signalling in L-DOPA-Induced Dyskinesia</article-title>
<alt-title alt-title-type="running-head">DARPP-32 and ERK in Dyskinesia</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Santini</surname>
<given-names>Emanuela</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sgambato-Faure</surname>
<given-names>Veronique</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Qin</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Savasta</surname>
<given-names>Marc</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dovero</surname>
<given-names>Sandra</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fisone</surname>
<given-names>Gilberto</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bezard</surname>
<given-names>Erwan</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>1</label>
<addr-line>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden</addr-line>
</aff>
<aff id="aff2"><label>2</label>
<addr-line>INSERM U836, Grenoble Institut des Neurosciences, Grenoble, France</addr-line>
</aff>
<aff id="aff3"><label>3</label>
<addr-line>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique UMR 5229 - Université Claude Bernard Lyon I, Bron, France</addr-line>
</aff>
<aff id="aff4"><label>4</label>
<addr-line>Université Victor Segalen-Bordeaux 2, Centre National de la Recherche Scientifique, Bordeaux Institute of Neuroscience, UMR 5227, Bordeaux, France</addr-line>
</aff>
<aff id="aff5"><label>5</label>
<addr-line>Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China</addr-line>
</aff>
<contrib-group><contrib contrib-type="editor"><name><surname>Cookson</surname>
<given-names>Mark R.</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1">National Institutes of Health, United States of America</aff>
<author-notes><corresp id="cor1">* E-mail: <email>erwan.bezard@u-bordeaux2.fr</email>
</corresp>
<fn fn-type="con"><p>Conceived and designed the experiments: GF EB. Performed the experiments: ES VSF QL MS SD GF EB. Analyzed the data: VSF QL MS SD GF EB. Wrote the paper: ES GF EB.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2010</year>
</pub-date>
<pub-date pub-type="epub"><day>23</day>
<month>8</month>
<year>2010</year>
</pub-date>
<volume>5</volume>
<issue>8</issue>
<elocation-id>e12322</elocation-id>
<history><date date-type="received"><day>21</day>
<month>6</month>
<year>2010</year>
</date>
<date date-type="accepted"><day>30</day>
<month>7</month>
<year>2010</year>
</date>
</history>
<permissions><copyright-statement>Santini et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</copyright-statement>
</permissions>
<abstract><sec><title>Background</title>
<p>In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. However, very little is known, in non-human primates, about the regulation of these signalling cascades and their association with the induction, manifestation and/or maintenance of dyskinesia.</p>
</sec>
<sec><title>Methodology/Results</title>
<p>We here studied, in the gold-standard non-human primate model of Parkinson's disease, the changes in PKA-dependent phosphorylation of DARPP-32 and GluR1 AMPA receptor, as well as in ERK and ribosomal protein S6 (S6) phosphorylation, associated to acute and chronic administration of L-DOPA. Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. In contrast, phosphorylation of ERK and S6 was enhanced preferentially after acute L-DOPA administration and decreased during the course of chronic treatment.</p>
</sec>
<sec><title>Conclusion</title>
<p>Dysregulation of cAMP signalling is maintained during the course of chronic L-DOPA administration, while abnormal ERK signalling peaks during the initial phase of L-DOPA treatment and decreases following prolonged exposure. While cAMP signalling enhancement is associated with dyskinesia, abnormal ERK signalling is associated with priming.</p>
</sec>
</abstract>
<counts><page-count count="5"></page-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>France</li>
<li>République populaire de Chine</li>
<li>Suède</li>
</country>
<region><li>Aquitaine</li>
<li>Auvergne-Rhône-Alpes</li>
<li>Nouvelle-Aquitaine</li>
<li>Rhône-Alpes</li>
<li>Svealand</li>
</region>
<settlement><li>Bordeaux</li>
<li>Grenoble</li>
<li>Pékin</li>
<li>Stockholm</li>
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<tree><country name="Suède"><region name="Svealand"><name sortKey="Santini, Emanuela" sort="Santini, Emanuela" uniqKey="Santini E" first="Emanuela" last="Santini">Emanuela Santini</name>
</region>
<name sortKey="Fisone, Gilberto" sort="Fisone, Gilberto" uniqKey="Fisone G" first="Gilberto" last="Fisone">Gilberto Fisone</name>
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<country name="France"><region name="Auvergne-Rhône-Alpes"><name sortKey="Sgambato Faure, Veronique" sort="Sgambato Faure, Veronique" uniqKey="Sgambato Faure V" first="Veronique" last="Sgambato-Faure">Veronique Sgambato-Faure</name>
</region>
<name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
<name sortKey="Dovero, Sandra" sort="Dovero, Sandra" uniqKey="Dovero S" first="Sandra" last="Dovero">Sandra Dovero</name>
<name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name>
<name sortKey="Savasta, Marc" sort="Savasta, Marc" uniqKey="Savasta M" first="Marc" last="Savasta">Marc Savasta</name>
<name sortKey="Sgambato Faure, Veronique" sort="Sgambato Faure, Veronique" uniqKey="Sgambato Faure V" first="Veronique" last="Sgambato-Faure">Veronique Sgambato-Faure</name>
</country>
<country name="République populaire de Chine"><noRegion><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name>
</noRegion>
<name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
</country>
</tree>
</affiliations>
</record>
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