ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.
Identifieur interne : 000585 ( PubMed/Curation ); précédent : 000584; suivant : 000586ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.
Auteurs : Danhui Zhang [États-Unis] ; Tanuja Bordia ; Matthew Mcgregor ; J Michael Mcintosh ; Michael W. Decker ; Maryka QuikSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Dyskinesia, Drug-Induced (drug therapy), Female, Levodopa (adverse effects), Levodopa (therapeutic use), MPTP Poisoning (drug therapy), Male, Nicotinic Agonists (therapeutic use), Pyridines (therapeutic use), Pyrrolidines (therapeutic use), Saimiri, Treatment Outcome.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa, Nicotinic Agonists, Pyridines, Pyrrolidines.
- drug therapy : Dyskinesia, Drug-Induced, MPTP Poisoning.
- Animals, Female, Male, Saimiri, Treatment Outcome.
Abstract
Levodopa-induced dyskinesias (LIDs) are a serious complication of levodopa therapy for Parkinson's disease for which there is little treatment. Accumulating evidence shows that nicotinic acetylcholine receptor (nAChR) drugs decrease LIDs in parkinsonian animals. Here, we examined the effect of two β2 nAChR agonists, ABT-089 and ABT-894, that previously were approved for phase 2 clinical trials for other indications. Two sets of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys were administered levodopa/carbidopa (10 mg/kg and 2.5 mg/kg, respectively) twice daily 5 days a week until they were stably dyskinetic. Each set had a vehicle-treated group, an nAChR agonist-treated group, and a nicotine-treated group as a positive control. Set A monkeys had previously received other nAChR drugs (nAChR drug-primed), whereas Set B monkeys were initially nAChR drug-naive. Both sets were administered the partial agonist ABT-089 (range, 0.01-1.0 mg/kg) orally 5 days a week twice daily 30 minutes before levodopa with each dose given for 1 to 5 weeks. ABT-089 decreased LIDs by 30% to 50% compared with vehicle-treated monkeys. Nicotine reduced LIDs by 70% in a parallel group. After 4 weeks of washout, the effect of the full agonist ABT-894 (range, 0.0001-0.10 mg/kg) was assessed on LIDs in Set A and Set B. ABT-894 reduced LIDs by 70%, similar to nicotine. Both drugs acted equally well at α4β2* and α6β2* nAChRs; however, ABT-089 was 30 to 60 times less potent than ABT-894. Tolerance did not develop for the time periods tested (range, 3-4 months). The nAChR drugs did not worsen parkinsonism or cognitive ability. Emesis, a common problem with nAChR drugs, was not observed. ABT-894 and ABT-089 appear to be good candidate nAChR drugs for the management of LIDs in Parkinson's disease.
DOI: 10.1002/mds.25817
PubMed: 24515328
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.</title><author><name sortKey="Zhang, Danhui" sort="Zhang, Danhui" uniqKey="Zhang D" first="Danhui" last="Zhang">Danhui Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Center for Health Sciences, SRI International, Menlo Park, California, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Health Sciences, SRI International, Menlo Park, California</wicri:regionArea></affiliation></author><author><name sortKey="Bordia, Tanuja" sort="Bordia, Tanuja" uniqKey="Bordia T" first="Tanuja" last="Bordia">Tanuja Bordia</name></author><author><name sortKey="Mcgregor, Matthew" sort="Mcgregor, Matthew" uniqKey="Mcgregor M" first="Matthew" last="Mcgregor">Matthew Mcgregor</name></author><author><name sortKey="Mcintosh, J Michael" sort="Mcintosh, J Michael" uniqKey="Mcintosh J" first="J Michael" last="Mcintosh">J Michael Mcintosh</name></author><author><name sortKey="Decker, Michael W" sort="Decker, Michael W" uniqKey="Decker M" first="Michael W" last="Decker">Michael W. Decker</name></author><author><name sortKey="Quik, Maryka" sort="Quik, Maryka" uniqKey="Quik M" first="Maryka" last="Quik">Maryka Quik</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24515328</idno><idno type="pmid">24515328</idno><idno type="doi">10.1002/mds.25817</idno><idno type="wicri:Area/PubMed/Corpus">000585</idno><idno type="wicri:Area/PubMed/Curation">000585</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.</title><author><name sortKey="Zhang, Danhui" sort="Zhang, Danhui" uniqKey="Zhang D" first="Danhui" last="Zhang">Danhui Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Center for Health Sciences, SRI International, Menlo Park, California, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Health Sciences, SRI International, Menlo Park, California</wicri:regionArea></affiliation></author><author><name sortKey="Bordia, Tanuja" sort="Bordia, Tanuja" uniqKey="Bordia T" first="Tanuja" last="Bordia">Tanuja Bordia</name></author><author><name sortKey="Mcgregor, Matthew" sort="Mcgregor, Matthew" uniqKey="Mcgregor M" first="Matthew" last="Mcgregor">Matthew Mcgregor</name></author><author><name sortKey="Mcintosh, J Michael" sort="Mcintosh, J Michael" uniqKey="Mcintosh J" first="J Michael" last="Mcintosh">J Michael Mcintosh</name></author><author><name sortKey="Decker, Michael W" sort="Decker, Michael W" uniqKey="Decker M" first="Michael W" last="Decker">Michael W. Decker</name></author><author><name sortKey="Quik, Maryka" sort="Quik, Maryka" uniqKey="Quik M" first="Maryka" last="Quik">Maryka Quik</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="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Female</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>MPTP Poisoning (drug therapy)</term><term>Male</term><term>Nicotinic Agonists (therapeutic use)</term><term>Pyridines (therapeutic use)</term><term>Pyrrolidines (therapeutic use)</term><term>Saimiri</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term><term>Nicotinic Agonists</term><term>Pyridines</term><term>Pyrrolidines</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Male</term><term>Saimiri</term><term>Treatment Outcome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Levodopa-induced dyskinesias (LIDs) are a serious complication of levodopa therapy for Parkinson's disease for which there is little treatment. Accumulating evidence shows that nicotinic acetylcholine receptor (nAChR) drugs decrease LIDs in parkinsonian animals. Here, we examined the effect of two β2 nAChR agonists, ABT-089 and ABT-894, that previously were approved for phase 2 clinical trials for other indications. Two sets of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys were administered levodopa/carbidopa (10 mg/kg and 2.5 mg/kg, respectively) twice daily 5 days a week until they were stably dyskinetic. Each set had a vehicle-treated group, an nAChR agonist-treated group, and a nicotine-treated group as a positive control. Set A monkeys had previously received other nAChR drugs (nAChR drug-primed), whereas Set B monkeys were initially nAChR drug-naive. Both sets were administered the partial agonist ABT-089 (range, 0.01-1.0 mg/kg) orally 5 days a week twice daily 30 minutes before levodopa with each dose given for 1 to 5 weeks. ABT-089 decreased LIDs by 30% to 50% compared with vehicle-treated monkeys. Nicotine reduced LIDs by 70% in a parallel group. After 4 weeks of washout, the effect of the full agonist ABT-894 (range, 0.0001-0.10 mg/kg) was assessed on LIDs in Set A and Set B. ABT-894 reduced LIDs by 70%, similar to nicotine. Both drugs acted equally well at α4β2* and α6β2* nAChRs; however, ABT-089 was 30 to 60 times less potent than ABT-894. Tolerance did not develop for the time periods tested (range, 3-4 months). The nAChR drugs did not worsen parkinsonism or cognitive ability. Emesis, a common problem with nAChR drugs, was not observed. ABT-894 and ABT-089 appear to be good candidate nAChR drugs for the management of LIDs in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24515328</PMID><DateCreated><Year>2014</Year><Month>04</Month><Day>04</Day></DateCreated><DateCompleted><Year>2014</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2015</Year><Month>04</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>4</Issue><PubDate><Year>2014</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>ABT-089 and ABT-894 reduce levodopa-induced dyskinesias in a monkey model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>508-17</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25817</ELocationID><Abstract><AbstractText>Levodopa-induced dyskinesias (LIDs) are a serious complication of levodopa therapy for Parkinson's disease for which there is little treatment. Accumulating evidence shows that nicotinic acetylcholine receptor (nAChR) drugs decrease LIDs in parkinsonian animals. Here, we examined the effect of two β2 nAChR agonists, ABT-089 and ABT-894, that previously were approved for phase 2 clinical trials for other indications. Two sets of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys were administered levodopa/carbidopa (10 mg/kg and 2.5 mg/kg, respectively) twice daily 5 days a week until they were stably dyskinetic. Each set had a vehicle-treated group, an nAChR agonist-treated group, and a nicotine-treated group as a positive control. Set A monkeys had previously received other nAChR drugs (nAChR drug-primed), whereas Set B monkeys were initially nAChR drug-naive. Both sets were administered the partial agonist ABT-089 (range, 0.01-1.0 mg/kg) orally 5 days a week twice daily 30 minutes before levodopa with each dose given for 1 to 5 weeks. ABT-089 decreased LIDs by 30% to 50% compared with vehicle-treated monkeys. Nicotine reduced LIDs by 70% in a parallel group. After 4 weeks of washout, the effect of the full agonist ABT-894 (range, 0.0001-0.10 mg/kg) was assessed on LIDs in Set A and Set B. ABT-894 reduced LIDs by 70%, similar to nicotine. Both drugs acted equally well at α4β2* and α6β2* nAChRs; however, ABT-089 was 30 to 60 times less potent than ABT-894. Tolerance did not develop for the time periods tested (range, 3-4 months). The nAChR drugs did not worsen parkinsonism or cognitive ability. Emesis, a common problem with nAChR drugs, was not observed. ABT-894 and ABT-089 appear to be good candidate nAChR drugs for the management of LIDs in Parkinson's disease.</AbstractText><CopyrightInformation>© 2014 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Danhui</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Center for Health Sciences, SRI International, Menlo Park, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordia</LastName><ForeName>Tanuja</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>McGregor</LastName><ForeName>Matthew</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>McIntosh</LastName><ForeName>J Michael</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Decker</LastName><ForeName>Michael W</ForeName><Initials>MW</Initials></Author><Author ValidYN="Y"><LastName>Quik</LastName><ForeName>Maryka</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>GM103801</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>GM48677</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS59910</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS059910</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>02</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018722">Nicotinic Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011725">Pyridines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011759">Pyrrolidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>CL2002R563</RegistryNumber><NameOfSubstance UI="C108326">pozanicline</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neuropharmacology. 2009 Jan;56(1):237-46</RefSource><PMID Version="1">18723036</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Pharmacol. 2013 Oct 15;86(8):1153-62</RefSource><PMID Version="1">23831952</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biol Pharm Bull. 2009 Mar;32(3):332-6</RefSource><PMID Version="1">19252273</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2009 Aug;63(8):653-61</RefSource><PMID Version="1">19347958</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2009 Jul 15;24(9):1255-66</RefSource><PMID Version="1">19412960</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Pharmacol. 2009 Oct 1;78(7):795-802</RefSource><PMID Version="1">19481067</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Pharmacol. 2009 Oct 1;78(7):844-51</RefSource><PMID Version="1">19555668</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2000 Oct 15;20(20):7816-21</RefSource><PMID Version="1">11027246</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2001 Aug 1;21(15):5494-500</RefSource><PMID Version="1">11466420</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2002 Apr;81(2):403-6</RefSource><PMID Version="1">12064487</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2002 Sep;17(5):902-9</RefSource><PMID Version="1">12360538</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Pharmacol. 2003 May;63(5):1169-79</RefSource><PMID Version="1">12695545</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2004 Apr 7;24(14):3655-62</RefSource><PMID Version="1">15071114</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Pharmacol Sci. 2004 Jun;25(6):317-24</RefSource><PMID Version="1">15165747</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 1997 Oct;283(1):235-46</RefSource><PMID Version="1">9336329</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2010 Jul;64(7):511-9</RefSource><PMID Version="1">20196140</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 2010 Jun;333(3):929-38</RefSource><PMID Version="1">20200117</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2010 Jul 29;466(7306):622-6</RefSource><PMID Version="1">20613723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Biobehav Rev. 2010 Nov;35(2):220-31</RefSource><PMID Version="1">20170672</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropharmacology. 2011 May;60(6):861-8</RefSource><PMID Version="1">21232546</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Alzheimers Dis. 2011;24 Suppl 2:95-109</RefSource><PMID Version="1">21403387</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2011 Jun;36(7):1319-31</RefSource><PMID Version="1">21412223</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2011 May;26(6):1072-82</RefSource><PMID Version="1">21626552</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2011 Aug;25(8):2563-73</RefSource><PMID Version="1">21507900</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 2011 Sep;338(3):932-41</RefSource><PMID Version="1">21665941</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int Rev Neurobiol. 2011;98:123-50</RefSource><PMID Version="1">21907085</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pharmacol Rev. 2011 Dec;63(4):938-66</RefSource><PMID Version="1">21969327</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2011 Nov 10;195:21-36</RefSource><PMID Version="1">21884762</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm. 2011 Dec;118(12):1661-90</RefSource><PMID Version="1">21881839</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S123-5</RefSource><PMID Version="1">22166408</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Expert Opin Investig Drugs. 2012 Feb;21(2):153-68</RefSource><PMID Version="1">22233485</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Psychopharmacology (Berl). 2012 Feb;219(3):715-25</RefSource><PMID Version="1">21748252</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2012 Jan;96(1):69-86</RefSource><PMID Version="1">22075179</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pain. 2012 Apr;153(4):862-8</RefSource><PMID Version="1">22386472</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 1997 Oct;283(1):247-58</RefSource><PMID Version="1">9336330</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2006 Sep;98(6):1866-75</RefSource><PMID Version="1">16882311</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm. 2007 Jan;114(1):135-47</RefSource><PMID Version="1">16906354</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Psychopharmacology (Berl). 2007 Feb;190(3):269-319</RefSource><PMID Version="1">16896961</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Med Chem. 2007 Nov 1;50(22):5493-508</RefSource><PMID Version="1">17929796</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Front Biosci. 2008;13:492-504</RefSource><PMID Version="1">17981563</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2007 Dec;62(6):588-96</RefSource><PMID Version="1">17960553</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FEBS J. 2008 Apr;275(7):1392-9</RefSource><PMID Version="1">18279379</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2008 Jun;85(2):135-47</RefSource><PMID Version="1">18482793</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2008;172:361-83</RefSource><PMID Version="1">18772042</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2008;172:465-78</RefSource><PMID Version="1">18772046</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Pharmacol. 2008 Dec 14;600(1-3):93-7</RefSource><PMID Version="1">18950618</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Neurol. 2012 Aug;25(4):448-59</RefSource><PMID Version="1">22772874</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Psychiatry. 2012 Jun;73(6):783-9</RefSource><PMID Version="1">22795204</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 2012 Aug;342(2):327-34</RefSource><PMID Version="1">22550286</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2012 Jul;27(8):947-57</RefSource><PMID Version="1">22693036</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Pharm Sci. 2012 Dec 18;47(5):813-23</RefSource><PMID Version="1">23036283</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>CNS Drugs. 2012 Dec;26(12):1017-32</RefSource><PMID Version="1">23114872</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2013 Feb;50:30-41</RefSource><PMID Version="1">23009753</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Pharmacol Rev. 2013 Jan;65(1):171-222</RefSource><PMID Version="1">23319549</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2013 Feb;38(3):405-13</RefSource><PMID Version="1">23032073</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropharmacology. 2013 Aug;71:191-203</RefSource><PMID Version="1">23583932</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropharmacology. 2013 Oct;73:337-47</RefSource><PMID Version="1">23770260</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 2013 Oct;347(1):225-34</RefSource><PMID Version="1">23902940</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2013 Sep;28(10):1398-406</RefSource><PMID Version="1">23836409</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Physiol Rev. 2009 Jan;89(1):73-120</RefSource><PMID Version="1">19126755</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004409">Dyskinesia, Drug-Induced</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020267">MPTP Poisoning</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018722">Nicotinic Agonists</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011725">Pyridines</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011759">Pyrrolidines</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012453">Saimiri</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016896">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS557408</OtherID><OtherID Source="NLM">PMC3990279</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ABT-089</Keyword><Keyword MajorTopicYN="N">ABT-894</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">dyskinesia</Keyword><Keyword MajorTopicYN="N">levodopa</Keyword><Keyword MajorTopicYN="N">nicotinic</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>12</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>12</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>2</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24515328</ArticleId><ArticleId IdType="doi">10.1002/mds.25817</ArticleId><ArticleId IdType="pmc">PMC3990279</ArticleId><ArticleId 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