Embryonic mesencephalic grafts increase levodopa-induced forelimb hyperkinesia in parkinsonian rats.
Identifieur interne : 003608 ( PubMed/Corpus ); précédent : 003607; suivant : 003609Embryonic mesencephalic grafts increase levodopa-induced forelimb hyperkinesia in parkinsonian rats.
Auteurs : Kathy Steece-Collier ; Timothy J. Collier ; Paul D. Danielson ; Roger Kurlan ; David M. Yurek ; John R. SladekSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Disease Models, Animal, Dopamine (metabolism), Forelimb (physiopathology), Hyperkinesis (chemically induced), Hyperkinesis (physiopathology), Levodopa (adverse effects), Levodopa (therapeutic use), Male, Mesencephalon (embryology), Mesencephalon (metabolism), Mesencephalon (transplantation), Neurons (metabolism), Neurons (transplantation), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (surgery), Postoperative Complications, Rats, Rats, Inbred F344.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , metabolism : Dopamine.
- chemically induced : Hyperkinesis.
- drug therapy : Parkinson Disease.
- embryology : Mesencephalon.
- metabolism : Mesencephalon, Neurons.
- physiopathology : Forelimb, Hyperkinesis, Parkinson Disease.
- surgery : Parkinson Disease.
- chemical , therapeutic use : Levodopa.
- transplantation : Mesencephalon, Neurons.
- Animals, Disease Models, Animal, Male, Postoperative Complications, Rats, Rats, Inbred F344.
Abstract
Recent observations from clinical trials of neural grafting for Parkinson's disease (PD) have demonstrated that grafted dopamine neurons can worsen dyskinesias in some graft recipients. This deleterious side effect reveals a new challenge for neural transplantation, that of elucidating mechanisms underlying these postgraft dyskinesias. One problem facing this challenge is the availability of a cost-effective and reliable animal model in which to pursue initial investigations. In the current study, we investigated the interaction of an embryonic ventral mesencephalic (VM) dopamine (DA) neuron graft on levodopa (LD)-induced dyskinetic movements in unilaterally 6-hydroxydopamine-lesioned rats. Rats were administered LD (levodopa-carbidopa, 50:5 mg/kg) twice daily for 6 weeks after either a sham graft or VM DA graft. Although a single solid graft of embryonic DA neurons can prevent progression of some lesioned-induced behavioral abnormalities such as LD-induced rotation and dystonia, it significantly increases hyperkinetic movements of the contralateral forelimb. This differential effect of grafted neurons on abnormal behavioral profiles is reminiscent of that reported in grafted patients with PD. Data from this study illustrate important similarities between this model of parkinsonism and PD in human patients that make it suitable for initial preclinical investigations into possible mechanisms underlying postgraft aggravation of dyskinetic movements.
DOI: 10.1002/mds.10588
PubMed: 14673880
Links to Exploration step
pubmed:14673880Le document en format XML
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Danielson</name></author><author><name sortKey="Kurlan, Roger" sort="Kurlan, Roger" uniqKey="Kurlan R" first="Roger" last="Kurlan">Roger Kurlan</name></author><author><name sortKey="Yurek, David M" sort="Yurek, David M" uniqKey="Yurek D" first="David M" last="Yurek">David M. Yurek</name></author><author><name sortKey="Sladek, John R" sort="Sladek, John R" uniqKey="Sladek J" first="John R" last="Sladek">John R. Sladek</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:14673880</idno><idno type="pmid">14673880</idno><idno type="doi">10.1002/mds.10588</idno><idno type="wicri:Area/PubMed/Corpus">003608</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Embryonic mesencephalic grafts increase levodopa-induced forelimb hyperkinesia in parkinsonian rats.</title><author><name sortKey="Steece Collier, Kathy" sort="Steece Collier, Kathy" uniqKey="Steece Collier K" first="Kathy" last="Steece-Collier">Kathy Steece-Collier</name><affiliation><nlm:affiliation>Department of Neurological Science, Research Center for Brain Repair, Rush Presbyterian St Luke's Medical Center, Chicago, Illinois 60612, USA. kathy_a_steece-collier@rush.edu</nlm:affiliation></affiliation></author><author><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J" last="Collier">Timothy J. Collier</name></author><author><name sortKey="Danielson, Paul D" sort="Danielson, Paul D" uniqKey="Danielson P" first="Paul D" last="Danielson">Paul D. Danielson</name></author><author><name sortKey="Kurlan, Roger" sort="Kurlan, Roger" uniqKey="Kurlan R" first="Roger" last="Kurlan">Roger Kurlan</name></author><author><name sortKey="Yurek, David M" sort="Yurek, David M" uniqKey="Yurek D" first="David M" last="Yurek">David M. Yurek</name></author><author><name sortKey="Sladek, John R" sort="Sladek, John R" uniqKey="Sladek J" first="John R" last="Sladek">John R. Sladek</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Forelimb (physiopathology)</term><term>Hyperkinesis (chemically induced)</term><term>Hyperkinesis (physiopathology)</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Mesencephalon (embryology)</term><term>Mesencephalon (metabolism)</term><term>Mesencephalon (transplantation)</term><term>Neurons (metabolism)</term><term>Neurons (transplantation)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (surgery)</term><term>Postoperative Complications</term><term>Rats</term><term>Rats, Inbred F344</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="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Hyperkinesis</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Mesencephalon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mesencephalon</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Forelimb</term><term>Hyperkinesis</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="transplantation" xml:lang="en"><term>Mesencephalon</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Male</term><term>Postoperative Complications</term><term>Rats</term><term>Rats, Inbred F344</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent observations from clinical trials of neural grafting for Parkinson's disease (PD) have demonstrated that grafted dopamine neurons can worsen dyskinesias in some graft recipients. This deleterious side effect reveals a new challenge for neural transplantation, that of elucidating mechanisms underlying these postgraft dyskinesias. One problem facing this challenge is the availability of a cost-effective and reliable animal model in which to pursue initial investigations. In the current study, we investigated the interaction of an embryonic ventral mesencephalic (VM) dopamine (DA) neuron graft on levodopa (LD)-induced dyskinetic movements in unilaterally 6-hydroxydopamine-lesioned rats. Rats were administered LD (levodopa-carbidopa, 50:5 mg/kg) twice daily for 6 weeks after either a sham graft or VM DA graft. Although a single solid graft of embryonic DA neurons can prevent progression of some lesioned-induced behavioral abnormalities such as LD-induced rotation and dystonia, it significantly increases hyperkinetic movements of the contralateral forelimb. This differential effect of grafted neurons on abnormal behavioral profiles is reminiscent of that reported in grafted patients with PD. Data from this study illustrate important similarities between this model of parkinsonism and PD in human patients that make it suitable for initial preclinical investigations into possible mechanisms underlying postgraft aggravation of dyskinetic movements.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">14673880</PMID><DateCreated><Year>2003</Year><Month>12</Month><Day>15</Day></DateCreated><DateCompleted><Year>2004</Year><Month>04</Month><Day>28</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>18</Volume><Issue>12</Issue><PubDate><Year>2003</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Embryonic mesencephalic grafts increase levodopa-induced forelimb hyperkinesia in parkinsonian rats.</ArticleTitle><Pagination><MedlinePgn>1442-54</MedlinePgn></Pagination><Abstract><AbstractText>Recent observations from clinical trials of neural grafting for Parkinson's disease (PD) have demonstrated that grafted dopamine neurons can worsen dyskinesias in some graft recipients. This deleterious side effect reveals a new challenge for neural transplantation, that of elucidating mechanisms underlying these postgraft dyskinesias. One problem facing this challenge is the availability of a cost-effective and reliable animal model in which to pursue initial investigations. In the current study, we investigated the interaction of an embryonic ventral mesencephalic (VM) dopamine (DA) neuron graft on levodopa (LD)-induced dyskinetic movements in unilaterally 6-hydroxydopamine-lesioned rats. Rats were administered LD (levodopa-carbidopa, 50:5 mg/kg) twice daily for 6 weeks after either a sham graft or VM DA graft. Although a single solid graft of embryonic DA neurons can prevent progression of some lesioned-induced behavioral abnormalities such as LD-induced rotation and dystonia, it significantly increases hyperkinetic movements of the contralateral forelimb. This differential effect of grafted neurons on abnormal behavioral profiles is reminiscent of that reported in grafted patients with PD. Data from this study illustrate important similarities between this model of parkinsonism and PD in human patients that make it suitable for initial preclinical investigations into possible mechanisms underlying postgraft aggravation of dyskinetic movements.</AbstractText><CopyrightInformation>Copyright 2003 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Steece-Collier</LastName><ForeName>Kathy</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Neurological Science, Research Center for Brain Repair, Rush Presbyterian St Luke's Medical Center, Chicago, Illinois 60612, USA. kathy_a_steece-collier@rush.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Collier</LastName><ForeName>Timothy J</ForeName><Initials>TJ</Initials></Author><Author ValidYN="Y"><LastName>Danielson</LastName><ForeName>Paul D</ForeName><Initials>PD</Initials></Author><Author ValidYN="Y"><LastName>Kurlan</LastName><ForeName>Roger</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Yurek</LastName><ForeName>David M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Sladek</LastName><ForeName>John R</ForeName><Initials>JR</Initials><Suffix>Jr</Suffix></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></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>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><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></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005552">Forelimb</DescriptorName><QualifierName MajorTopicYN="Y" 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UI="Q000637">transplantation</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000637">transplantation</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000601">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D011183">Postoperative Complications</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011916">Rats, Inbred 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