Embryonic mesencephalic grafts increase levodopa‐induced forelimb hyperkinesia in parkinsonian rats
Identifieur interne : 004101 ( Main/Exploration ); précédent : 004100; suivant : 004102Embryonic mesencephalic grafts increase levodopa‐induced forelimb hyperkinesia in parkinsonian rats
Auteurs : Kathy Steece-Collier [États-Unis] ; Timothy J. Collier [États-Unis] ; Paul D. Danielson [États-Unis] ; Roger Kurlan [États-Unis] ; David M. Yurek [États-Unis] ; John R. Sladek Jr [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-12.
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), Parkinson's disease, Postoperative Complications, Rats, Rats, Inbred F344, animal models, dyskinesias, levodopa, neurotransplantation.
- 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. © 2003 Movement Disorder Society
Url:
DOI: 10.1002/mds.10588
Affiliations:
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-12">2003-12</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1442">1442</biblScope><biblScope unit="page" to="1454">1454</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B7BBC6AE2260B16DCE7AABF052A8AB57298193B0</idno><idno type="DOI">10.1002/mds.10588</idno><idno type="ArticleID">MDS10588</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></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>Parkinson's disease</term><term>Postoperative Complications</term><term>Rats</term><term>Rats, Inbred F344</term><term>animal models</term><term>dyskinesias</term><term>levodopa</term><term>neurotransplantation</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><langUsage><language ident="en">en</language></langUsage></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. © 2003 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li><li>Illinois</li><li>Kentucky</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="Illinois"><name sortKey="Steece Ollier, Kathy" sort="Steece Ollier, Kathy" uniqKey="Steece Ollier K" first="Kathy" last="Steece-Collier">Kathy Steece-Collier</name></region><name sortKey="Collier, Timothy J" sort="Collier, Timothy J" uniqKey="Collier T" first="Timothy J." last="Collier">Timothy J. Collier</name><name sortKey="Danielson, Paul D" sort="Danielson, Paul D" uniqKey="Danielson P" first="Paul D." last="Danielson">Paul D. Danielson</name><name sortKey="Kurlan, Roger" sort="Kurlan, Roger" uniqKey="Kurlan R" first="Roger" last="Kurlan">Roger Kurlan</name><name sortKey="Sladek Jr, John R" sort="Sladek Jr, John R" uniqKey="Sladek Jr J" first="John R." last="Sladek Jr">John R. Sladek Jr</name><name sortKey="Yurek, David M" sort="Yurek, David M" uniqKey="Yurek D" first="David M." last="Yurek">David M. Yurek</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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