Striatal histone modifications in models of levodopa-induced dyskinesia
Identifieur interne : 000673 ( PascalFrancis/Curation ); précédent : 000672; suivant : 000674Striatal 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.
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- Pascal (Inist)
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- topic : Singe.
English descriptors
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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.
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Standaert</name><affiliation wicri:level="1"><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></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">08-0317913</idno><date when="2008">2008</date><idno type="stanalyst">PASCAL 08-0317913 INIST</idno><idno type="RBID">Pascal:08-0317913</idno><idno type="wicri:Area/PascalFrancis/Corpus">000637</idno><idno type="wicri:Area/PascalFrancis/Curation">000673</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Striatal histone modifications in models of levodopa-induced dyskinesia</title><author><name sortKey="Nicholas, Anthony P" sort="Nicholas, Anthony P" uniqKey="Nicholas A" first="Anthony P." last="Nicholas">Anthony P. Nicholas</name><affiliation wicri:level="1"><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></affiliation><affiliation wicri:level="1"><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></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="1"><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></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="1"><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></affiliation></author><author><name sortKey="Vattem, Padmapriya" sort="Vattem, Padmapriya" uniqKey="Vattem P" first="Padmapriya" last="Vattem">Padmapriya Vattem</name><affiliation wicri:level="1"><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></affiliation></author><author><name sortKey="Ravenscroft, Paula" sort="Ravenscroft, Paula" uniqKey="Ravenscroft P" first="Paula" last="Ravenscroft">Paula Ravenscroft</name><affiliation wicri:level="1"><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></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation wicri:level="1"><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></affiliation></author><author><name sortKey="Shaobo Zhou" sort="Shaobo Zhou" uniqKey="Shaobo Zhou" last="Shaobo Zhou">SHAOBO ZHOU</name><affiliation wicri:level="1"><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></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></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></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="1"><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></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="1"><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></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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>106</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Striatal histone modifications in models of levodopa-induced dyskinesia</s1></fA08><fA11 i1="01" i2="1"><s1>NICHOLAS (Anthony P.)</s1></fA11><fA11 i1="02" i2="1"><s1>LUBIN (Farah D.)</s1></fA11><fA11 i1="03" i2="1"><s1>HALLETT (Penelope J.)</s1></fA11><fA11 i1="04" i2="1"><s1>VATTEM (Padmapriya)</s1></fA11><fA11 i1="05" i2="1"><s1>RAVENSCROFT (Paula)</s1></fA11><fA11 i1="06" i2="1"><s1>BEZARD (Erwan)</s1></fA11><fA11 i1="07" i2="1"><s1>SHAOBO ZHOU</s1></fA11><fA11 i1="08" i2="1"><s1>FOX (Susan H.)</s1></fA11><fA11 i1="09" i2="1"><s1>BROTCHIE (Jonathan M.)</s1></fA11><fA11 i1="10" i2="1"><s1>SWEATT (J. David)</s1></fA11><fA11 i1="11" i2="1"><s1>STANDAERT (David G.)</s1></fA11><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></fA14><fA14 i1="02"><s1>Birmingham Veterans Administration Medical Center</s1><s2>Birmingham, Alabama</s2><s3>USA</s3><sZ>1 aut.</sZ></fA14><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></fA14><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></fA14><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></fA14><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></fA14><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></fA14><fA20><s1>486-494</s1></fA20><fA21><s1>2008</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000198033040410</s5></fA43><fA44><s0>0000</s0><s1>© 2008 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/2</s0></fA45><fA47 i1="01" i2="1"><s0>08-0317913</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17A01</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Corps strié</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Corpus striatum</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Cuerpo estriado</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Histone</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Histone</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Histona</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Modification</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Modification</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Modificación</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Modèle animal</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Animal 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l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="FRE"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="ENG"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="SPA"><s0>Primates</s0><s2>NS</s2></fC07><fN21><s1>196</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Striatal histone modifications in models of levodopa-induced dyskinesia
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