Striatal histone modifications in models of levodopa-induced dyskinesia
Identifieur interne : 000225 ( France/Analysis ); précédent : 000224; suivant : 000226Striatal histone modifications in models of levodopa-induced dyskinesia
Auteurs : Anthony P. Nicholas [États-Unis] ; Farah D. Lubin [États-Unis] ; Penelope J. Hallett [États-Unis] ; Padmapriya Vattem [États-Unis] ; Paula Ravenscroft [Royaume-Uni] ; Erwan Bezard [France] ; SHAOBO ZHOU [Royaume-Uni] ; Susan H. Fox [Canada] ; Jonathan M. Brotchie [Canada] ; J. David Sweatt [États-Unis] ; David G. Standaert [États-Unis]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2008.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
Abstract
Despite recent advances in the treatment of Parkinson disease (PD), levodopa remains the most effective and widely used therapy. A major limitation to the use of levodopa is the development of abnormal involuntary movements, termed levodopa-induced dyskinesia (LDID), following chronic levodopa treatment. Since recent studies have suggested that modifications of chromatin structure may be responsible for many long-lasting changes in brain function, we have examined post-translational modifications of striatal histones in two models of LDID: an acute murine model and a chronic macaque monkey model, both exposed to 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP). In the primate model, which closely resembles human LDID, we observed that chronic levodopa and the appearance of LDID was associated with marked deacetylation of histone H4, hyperacetylation and dephosphorylation of histone H3, and enhancement of the phosphorylation of extracellular signal-regulated kinase (ERK). In the murine model of acutely rather than chronically induced LDID, dopamine depletion and levodopa treatment also induced deacetylation of histone H4 and phosphorylation of ERK, but histone H3 exhibited decreased trimethylation and reduced rather than enhanced acetylation. These data demonstrate striking changes in striatal histones associated with the induction of LDID in both animal models. The pattern of changes observed, as well as the behavioral features, differed in the two models. However, both models exhibit marked deacetylation of histone H4, suggesting that inhibitors of H4 deacetylation may be useful in preventing or reversing LDID.
Affiliations:
- Canada, France, Royaume-Uni, États-Unis
- Alabama, Angleterre, Aquitaine, Grand Manchester, Massachusetts, Nouvelle-Aquitaine
- Bordeaux, Manchester
- Université de Manchester
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Nicholas</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Birmingham Veterans Administration Medical Center</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Lubin, Farah D" sort="Lubin, Farah D" uniqKey="Lubin F" first="Farah D." last="Lubin">Farah D. Lubin</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurobiology, University of Alabama at Birmingham</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J." last="Hallett">Penelope J. Hallett</name><affiliation wicri:level="2"><inist:fA14 i1="04"><s1>Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School</s1><s2>Charlestown, Massachusetts</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Vattem, Padmapriya" sort="Vattem, Padmapriya" uniqKey="Vattem P" first="Padmapriya" last="Vattem">Padmapriya Vattem</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Ravenscroft, Paula" sort="Ravenscroft, Paula" uniqKey="Ravenscroft P" first="Paula" last="Ravenscroft">Paula Ravenscroft</name><affiliation wicri:level="4"><inist:fA14 i1="05"><s1>School of Biological Sciences, University of Manchester</s1><s2>Manchester</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Manchester</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Manchester</region><settlement type="city">Manchester</settlement></placeName><orgName type="university">Université de Manchester</orgName></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation wicri:level="3"><inist:fA14 i1="06"><s1>Université Victor Segalen Bordeaux 2, Centre National de la Recherche Scientifique, Bordeaux Institute of Neuroscience, UMR 5227</s1><s2>Bordeaux</s2><s3>FRA</s3><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Nouvelle-Aquitaine</region><region type="old region">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Shaobo Zhou" sort="Shaobo Zhou" uniqKey="Shaobo Zhou" last="Shaobo Zhou">SHAOBO ZHOU</name><affiliation wicri:level="4"><inist:fA14 i1="05"><s1>School of Biological Sciences, University of Manchester</s1><s2>Manchester</s2><s3>GBR</s3><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Manchester</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Manchester</region><settlement type="city">Manchester</settlement></placeName><orgName type="university">Université de Manchester</orgName></affiliation></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Toronto Western Research Institute, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Toronto Western Research Institute, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Sweatt, J David" sort="Sweatt, J David" uniqKey="Sweatt J" first="J. David" last="Sweatt">J. David Sweatt</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurobiology, University of Alabama at Birmingham</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Standaert, David G" sort="Standaert, David G" uniqKey="Standaert D" first="David G." last="Standaert">David G. Standaert</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Alabama</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormal movement</term><term>Acute</term><term>Animal model</term><term>Chronic</term><term>Corpus striatum</term><term>Development</term><term>Dyskinesia</term><term>Encephalon</term><term>Histone</term><term>Involuntary movement</term><term>Levodopa</term><term>Modification</term><term>Monkey</term><term>Mouse</term><term>Parkinson disease</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Corps strié</term><term>Histone</term><term>Modification</term><term>Modèle animal</term><term>Lévodopa</term><term>Traitement</term><term>Développement</term><term>Mouvement anormal</term><term>Dyskinésie</term><term>Mouvement involontaire</term><term>Chronique</term><term>Maladie de Parkinson</term><term>Encéphale</term><term>Aigu</term><term>Souris</term><term>Singe</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite recent advances in the treatment of Parkinson disease (PD), levodopa remains the most effective and widely used therapy. A major limitation to the use of levodopa is the development of abnormal involuntary movements, termed levodopa-induced dyskinesia (LDID), following chronic levodopa treatment. Since recent studies have suggested that modifications of chromatin structure may be responsible for many long-lasting changes in brain function, we have examined post-translational modifications of striatal histones in two models of LDID: an acute murine model and a chronic macaque monkey model, both exposed to 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP). In the primate model, which closely resembles human LDID, we observed that chronic levodopa and the appearance of LDID was associated with marked deacetylation of histone H4, hyperacetylation and dephosphorylation of histone H3, and enhancement of the phosphorylation of extracellular signal-regulated kinase (ERK). In the murine model of acutely rather than chronically induced LDID, dopamine depletion and levodopa treatment also induced deacetylation of histone H4 and phosphorylation of ERK, but histone H3 exhibited decreased trimethylation and reduced rather than enhanced acetylation. These data demonstrate striking changes in striatal histones associated with the induction of LDID in both animal models. The pattern of changes observed, as well as the behavioral features, differed in the two models. However, both models exhibit marked deacetylation of histone H4, suggesting that inhibitors of H4 deacetylation may be useful in preventing or reversing LDID.</div></front></TEI><affiliations><list><country><li>Canada</li><li>France</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Alabama</li><li>Angleterre</li><li>Aquitaine</li><li>Grand Manchester</li><li>Massachusetts</li><li>Nouvelle-Aquitaine</li></region><settlement><li>Bordeaux</li><li>Manchester</li></settlement><orgName><li>Université de Manchester</li></orgName></list><tree><country name="États-Unis"><region name="Alabama"><name sortKey="Nicholas, Anthony P" sort="Nicholas, Anthony P" uniqKey="Nicholas A" first="Anthony P." last="Nicholas">Anthony P. Nicholas</name></region><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J." last="Hallett">Penelope J. Hallett</name><name sortKey="Lubin, Farah D" sort="Lubin, Farah D" uniqKey="Lubin F" first="Farah D." last="Lubin">Farah D. Lubin</name><name sortKey="Nicholas, Anthony P" sort="Nicholas, Anthony P" uniqKey="Nicholas A" first="Anthony P." last="Nicholas">Anthony P. Nicholas</name><name sortKey="Standaert, David G" sort="Standaert, David G" uniqKey="Standaert D" first="David G." last="Standaert">David G. Standaert</name><name sortKey="Sweatt, J David" sort="Sweatt, J David" uniqKey="Sweatt J" first="J. David" last="Sweatt">J. David Sweatt</name><name sortKey="Vattem, Padmapriya" sort="Vattem, Padmapriya" uniqKey="Vattem P" first="Padmapriya" last="Vattem">Padmapriya Vattem</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Ravenscroft, Paula" sort="Ravenscroft, Paula" uniqKey="Ravenscroft P" first="Paula" last="Ravenscroft">Paula Ravenscroft</name></region><name sortKey="Shaobo Zhou" sort="Shaobo Zhou" uniqKey="Shaobo Zhou" last="Shaobo Zhou">SHAOBO ZHOU</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></region></country><country name="Canada"><noRegion><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name></noRegion><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. 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