Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?
Identifieur interne : 001507 ( PubMed/Corpus ); précédent : 001506; suivant : 001508Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?
Auteurs : Morvarid Karimi ; Stephen M. Moerlein ; Tom O. Videen ; Robert R. Luedtke ; Michelle Taylor ; Robert H. Mach ; Joel S. PerlmutterSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Corpus Striatum (metabolism), Corpus Striatum (radionuclide imaging), Dystonic Disorders (pathology), Dystonic Disorders (radiography), Dystonic Disorders (radionuclide imaging), Female, Fluorine Radioisotopes (diagnostic use), Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Protein Binding (drug effects), Receptors, Dopamine D2 (metabolism).
- MESH :
- chemical , diagnostic use : Fluorine Radioisotopes.
- drug effects : Protein Binding.
- metabolism : Corpus Striatum, Receptors, Dopamine D2.
- pathology : Dystonic Disorders.
- radiography : Dystonic Disorders.
- radionuclide imaging : Corpus Striatum, Dystonic Disorders.
- Adult, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography.
Abstract
Dystonia is an involuntary movement disorder characterized by repetitive patterned or sustained muscle contractions causing twisting or abnormal postures. Several lines of evidence suggest that abnormalities of dopaminergic pathways contribute to the pathophysiology of dystonia. In particular, dysfunction of D2-like receptors that mediate function of the indirect pathway in the basal ganglia may play a key role. We have demonstrated with positron emission tomography that patients with primary focal cranial or hand dystonia have reduced putamenal specific binding of [(18)F]spiperone, a nonselective D2-like radioligand with nearly equal affinity for serotonergic 5-HT(2A) sites. We then repeated the study with [(18)F]N-methyl-benperidol (NMB), a more selective D2-like receptor radioligand with minimal affinity for 5-HT(2A). Surprisingly, there was no decrease in NMB binding in the putamen of subjects with dystonia. Our findings excluded reductions of putamenal uptake greater than 20% with 95% confidence intervals. The analysis of the in vitro selectivity of NMB and spiperone demonstrated that NMB was highly selective for D2 receptors relative to D3 receptors (200-fold difference in affinity), whereas spiperone has similar affinity for all three of the D2-like receptor subtypes. These findings when coupled with other literature suggest that a defect in D3, rather than D2, receptor expression may be associated with primary focal dystonia.
DOI: 10.1002/mds.23401
PubMed: 20960437
Links to Exploration step
pubmed:20960437Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?</title><author><name sortKey="Karimi, Morvarid" sort="Karimi, Morvarid" uniqKey="Karimi M" first="Morvarid" last="Karimi">Morvarid Karimi</name><affiliation><nlm:affiliation>Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri 63110-1093, USA. morvaridk@npg.wustl.edu</nlm:affiliation></affiliation></author><author><name sortKey="Moerlein, Stephen M" sort="Moerlein, Stephen M" uniqKey="Moerlein S" first="Stephen M" last="Moerlein">Stephen M. Moerlein</name></author><author><name sortKey="Videen, Tom O" sort="Videen, Tom O" uniqKey="Videen T" first="Tom O" last="Videen">Tom O. Videen</name></author><author><name sortKey="Luedtke, Robert R" sort="Luedtke, Robert R" uniqKey="Luedtke R" first="Robert R" last="Luedtke">Robert R. Luedtke</name></author><author><name sortKey="Taylor, Michelle" sort="Taylor, Michelle" uniqKey="Taylor M" first="Michelle" last="Taylor">Michelle Taylor</name></author><author><name sortKey="Mach, Robert H" sort="Mach, Robert H" uniqKey="Mach R" first="Robert H" last="Mach">Robert H. Mach</name></author><author><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S" last="Perlmutter">Joel S. Perlmutter</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="doi">10.1002/mds.23401</idno><idno type="RBID">pubmed:20960437</idno><idno type="pmid">20960437</idno><idno type="wicri:Area/PubMed/Corpus">001507</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?</title><author><name sortKey="Karimi, Morvarid" sort="Karimi, Morvarid" uniqKey="Karimi M" first="Morvarid" last="Karimi">Morvarid Karimi</name><affiliation><nlm:affiliation>Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri 63110-1093, USA. morvaridk@npg.wustl.edu</nlm:affiliation></affiliation></author><author><name sortKey="Moerlein, Stephen M" sort="Moerlein, Stephen M" uniqKey="Moerlein S" first="Stephen M" last="Moerlein">Stephen M. Moerlein</name></author><author><name sortKey="Videen, Tom O" sort="Videen, Tom O" uniqKey="Videen T" first="Tom O" last="Videen">Tom O. Videen</name></author><author><name sortKey="Luedtke, Robert R" sort="Luedtke, Robert R" uniqKey="Luedtke R" first="Robert R" last="Luedtke">Robert R. Luedtke</name></author><author><name sortKey="Taylor, Michelle" sort="Taylor, Michelle" uniqKey="Taylor M" first="Michelle" last="Taylor">Michelle Taylor</name></author><author><name sortKey="Mach, Robert H" sort="Mach, Robert H" uniqKey="Mach R" first="Robert H" last="Mach">Robert H. Mach</name></author><author><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S" last="Perlmutter">Joel S. Perlmutter</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (radionuclide imaging)</term><term>Dystonic Disorders (pathology)</term><term>Dystonic Disorders (radiography)</term><term>Dystonic Disorders (radionuclide imaging)</term><term>Female</term><term>Fluorine Radioisotopes (diagnostic use)</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term><term>Protein Binding (drug effects)</term><term>Receptors, Dopamine D2 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Fluorine Radioisotopes</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Protein Binding</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="radiography" xml:lang="en"><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Corpus Striatum</term><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dystonia is an involuntary movement disorder characterized by repetitive patterned or sustained muscle contractions causing twisting or abnormal postures. Several lines of evidence suggest that abnormalities of dopaminergic pathways contribute to the pathophysiology of dystonia. In particular, dysfunction of D2-like receptors that mediate function of the indirect pathway in the basal ganglia may play a key role. We have demonstrated with positron emission tomography that patients with primary focal cranial or hand dystonia have reduced putamenal specific binding of [(18)F]spiperone, a nonselective D2-like radioligand with nearly equal affinity for serotonergic 5-HT(2A) sites. We then repeated the study with [(18)F]N-methyl-benperidol (NMB), a more selective D2-like receptor radioligand with minimal affinity for 5-HT(2A). Surprisingly, there was no decrease in NMB binding in the putamen of subjects with dystonia. Our findings excluded reductions of putamenal uptake greater than 20% with 95% confidence intervals. The analysis of the in vitro selectivity of NMB and spiperone demonstrated that NMB was highly selective for D2 receptors relative to D3 receptors (200-fold difference in affinity), whereas spiperone has similar affinity for all three of the D2-like receptor subtypes. These findings when coupled with other literature suggest that a defect in D3, rather than D2, receptor expression may be associated with primary focal dystonia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20960437</PMID><DateCreated><Year>2011</Year><Month>02</Month><Day>15</Day></DateCreated><DateCompleted><Year>2011</Year><Month>06</Month><Day>06</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>1</Issue><PubDate><Year>2011</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?</ArticleTitle><Pagination><MedlinePgn>100-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23401</ELocationID><Abstract><AbstractText>Dystonia is an involuntary movement disorder characterized by repetitive patterned or sustained muscle contractions causing twisting or abnormal postures. Several lines of evidence suggest that abnormalities of dopaminergic pathways contribute to the pathophysiology of dystonia. In particular, dysfunction of D2-like receptors that mediate function of the indirect pathway in the basal ganglia may play a key role. We have demonstrated with positron emission tomography that patients with primary focal cranial or hand dystonia have reduced putamenal specific binding of [(18)F]spiperone, a nonselective D2-like radioligand with nearly equal affinity for serotonergic 5-HT(2A) sites. We then repeated the study with [(18)F]N-methyl-benperidol (NMB), a more selective D2-like receptor radioligand with minimal affinity for 5-HT(2A). Surprisingly, there was no decrease in NMB binding in the putamen of subjects with dystonia. Our findings excluded reductions of putamenal uptake greater than 20% with 95% confidence intervals. The analysis of the in vitro selectivity of NMB and spiperone demonstrated that NMB was highly selective for D2 receptors relative to D3 receptors (200-fold difference in affinity), whereas spiperone has similar affinity for all three of the D2-like receptor subtypes. These findings when coupled with other literature suggest that a defect in D3, rather than D2, receptor expression may be associated with primary focal dystonia.</AbstractText><CopyrightInformation>Copyright © 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Karimi</LastName><ForeName>Morvarid</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri 63110-1093, USA. morvaridk@npg.wustl.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moerlein</LastName><ForeName>Stephen M</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Videen</LastName><ForeName>Tom O</ForeName><Initials>TO</Initials></Author><Author ValidYN="Y"><LastName>Luedtke</LastName><ForeName>Robert R</ForeName><Initials>RR</Initials></Author><Author ValidYN="Y"><LastName>Taylor</LastName><ForeName>Michelle</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Mach</LastName><ForeName>Robert H</ForeName><Initials>RH</Initials></Author><Author ValidYN="Y"><LastName>Perlmutter</LastName><ForeName>Joel S</ForeName><Initials>JS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS031001</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS041509</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS050425</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS058714</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30NS05710</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United 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Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005462">Fluorine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017448">Receptors, Dopamine D2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Pharmacol. 2010 Feb;10(1):87-92</RefSource><PMID Version="1">19837631</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2010 Mar;37(3):558-73</RefSource><PMID Version="1">20005952</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2010 Jun;64(6):449-59</RefSource><PMID Version="1">20175227</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Comput Assist Tomogr. 1994 Jan-Feb;18(1):110-8</RefSource><PMID Version="1">8282858</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1993 Oct;116 ( Pt 5):1191-9</RefSource><PMID Version="1">8221055</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Phys Med Biol. 1996 Jan;41(1):153-76</RefSource><PMID Version="1">8685253</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1996 Mar;66(3):915-9</RefSource><PMID Version="1">8769849</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 1994 Oct;44(2):163-96</RefSource><PMID Version="1">7831476</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Nucl Med. 1995 Jul;36(7):1307-15</RefSource><PMID Version="1">7790961</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 1995 Jun;66(4):903-13</RefSource><PMID Version="1">7651617</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Neurol. 1995 Aug;8(4):310-3</RefSource><PMID Version="1">7582048</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2000 Mar;3(3):226-30</RefSource><PMID Version="1">10700253</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Neurosci. 2000;23:185-215</RefSource><PMID Version="1">10845063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2000 Dec 15;38(4):438-49</RefSource><PMID Version="1">11044891</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 2000 Oct;23(10 Suppl):S71-7</RefSource><PMID Version="1">11052223</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>IEEE Trans Med Imaging. 2000 Aug;19(8):809-14</RefSource><PMID Version="1">11055805</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurophysiol. 2000 Nov;84(5):2458-64</RefSource><PMID Version="1">11067988</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2000;125:277-90</RefSource><PMID Version="1">11098664</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2002 Aug 13;59(3):445-8</RefSource><PMID Version="1">12177384</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2003 Jan;84(2):373-81</RefSource><PMID Version="1">12558999</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 2003 May;74(5):665-6</RefSource><PMID Version="1">12700316</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 2004 Nov;27(11):662-9</RefSource><PMID Version="1">15474166</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Pharmacol. 1973 Dec 1;22(23):3099-108</RefSource><PMID Version="1">4202581</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Psychiatr Res. 1975 Nov;12(3):189-98</RefSource><PMID Version="1">1202204</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Psychopharmacologia. 1976 May 28;47(2):199-201</RefSource><PMID Version="1">5743</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1981 Apr;31(4):434-9</RefSource><PMID Version="1">6111766</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1985 Jun;108 ( Pt 2):463-83</RefSource><PMID Version="1">4005532</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Psychopharmacology (Berl). 1986;88(4):403-19</RefSource><PMID Version="1">2871578</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Neurosci. 1986;9:357-81</RefSource><PMID Version="1">3085570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1988 Jan;23(1):73-8</RefSource><PMID Version="1">3345068</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 1989;4 Suppl 1:S38-47</RefSource><PMID Version="1">2657409</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 1990 Jul;13(7):266-71</RefSource><PMID Version="1">1695401</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1990 Dec 7;250(4986):1429-32</RefSource><PMID Version="1">2147780</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1991 May;11(5):1381-9</RefSource><PMID Version="1">1827499</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 1992 Apr;15(4):133-9</RefSource><PMID Version="1">1374971</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int J Rad Appl Instrum A. 1992 Jul;43(7):913-7</RefSource><PMID Version="1">1321101</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Mol Brain Res. 1993 Apr;18(1-2):187-92</RefSource><PMID Version="1">8097550</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cereb Blood Flow Metab. 1996 Sep;16(5):834-40</RefSource><PMID Version="1">8784228</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucl Med Biol. 1997 May;24(4):311-8</RefSource><PMID Version="1">9257329</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cereb Blood Flow Metab. 1997 Aug;17(8):833-45</RefSource><PMID Version="1">9290581</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1997 Jan 15;17(2):843-50</RefSource><PMID Version="1">8987805</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1997 Nov;49(5):1432-8</RefSource><PMID Version="1">9371934</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Adv Neurol. 1998;78:1-10</RefSource><PMID Version="1">9750897</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 1999 Jan;20(1):60-80</RefSource><PMID Version="1">9885786</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 1960 Feb;23:56-62</RefSource><PMID Version="1">14399272</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2005 Jan 25;64(2):347-9</RefSource><PMID Version="1">15668438</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2005 Apr;20(4):395-402</RefSource><PMID Version="1">15719415</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>CNS Neurol Disord Drug Targets. 2006 Feb;5(1):25-43</RefSource><PMID Version="1">16613552</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2006 Sep 1;141(3):1281-7</RefSource><PMID Version="1">16766129</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Dev Neurosci. 2006;28(6):505-17</RefSource><PMID Version="1">17028428</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2007 Apr;13(3):170-3</RefSource><PMID Version="1">17107822</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2007 Aug;102(3):783-8</RefSource><PMID Version="1">17550429</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2007 Dec 7;282(49):35842-54</RefSource><PMID Version="1">17923483</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucl Med Biol. 2008 Apr;35(3):335-41</RefSource><PMID Version="1">18355689</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2008 Aug 8;321(5890):848-51</RefSource><PMID Version="1">18687967</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Sep 19;283(38):26016-25</RefSource><PMID Version="1">18644790</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2008 Oct 8;28(41):10363-9</RefSource><PMID Version="1">18842895</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2008 Oct;131(Pt 10):2710-9</RefSource><PMID Version="1">18697909</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2008 Oct;1142:179-99</RefSource><PMID Version="1">18990127</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2008 Nov 26;60(4):543-54</RefSource><PMID Version="1">19038213</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>CNS Neurol Disord Drug Targets. 2008 Nov;7(5):410-21</RefSource><PMID Version="1">19128200</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Nucl Med Mol Imaging. 2009 Feb;36(2):269-74</RefSource><PMID Version="1">18719906</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Behav Brain Res. 2009 Apr 12;199(1):129-40</RefSource><PMID Version="1">19135093</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2009 Apr;34(1):133-45</RefSource><PMID Version="1">19187797</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroimage. 2009 Jun;46(2):447-58</RefSource><PMID Version="1">19233294</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2009 Mar 15;24(4):490-9</RefSource><PMID Version="1">19185014</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2009 Jun 16;72(24):2097-103</RefSource><PMID Version="1">19528516</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2009 Oct;132(Pt 10):2871-7</RefSource><PMID 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Source="NLM">NIHMS225271</OtherID><OtherID Source="NLM">PMC3025272</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>4</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2010</Year><Month>6</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>7</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2010</Year><Month>10</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>6</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23401</ArticleId><ArticleId IdType="pubmed">20960437</ArticleId><ArticleId IdType="pmc">PMC3025272</ArticleId><ArticleId IdType="mid">NIHMS225271</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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