Genetic, temporal and diurnal influences on L-dopa-induced dyskinesia in the 6-OHDA model.
Identifieur interne : 000B16 ( PubMed/Checkpoint ); précédent : 000B15; suivant : 000B17Genetic, temporal and diurnal influences on L-dopa-induced dyskinesia in the 6-OHDA model.
Auteurs : Christelle Monville [France] ; Eduardo M. Torres ; Vladimir Pekarik ; Emma L. Lane ; Stephen B. DunnettSource :
- Brain research bulletin [ 1873-2747 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (therapeutic use), Antiparkinson Agents (toxicity), Circadian Rhythm (physiology), Disease Models, Animal, Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (genetics), Dyskinesia, Drug-Induced (physiopathology), Female, Injections, Intraperitoneal (methods), Levodopa (therapeutic use), Levodopa (toxicity), Microinjections (methods), Motor Activity (drug effects), Motor Activity (physiology), Oxidopamine (administration & dosage), Oxidopamine (toxicity), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Rats, Rats, Inbred Lew, Rats, Sprague-Dawley, Risk Factors, Rotation, Species Specificity, Sympatholytics (administration & dosage), Sympatholytics (toxicity), Time Factors, Treatment Outcome.
- MESH :
- chemical , administration & dosage : Oxidopamine, Sympatholytics.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- chemical , toxicity : Antiparkinson Agents, Levodopa, Oxidopamine, Sympatholytics.
- complications : Parkinson Disease.
- drug effects : Motor Activity.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- genetics : Dyskinesia, Drug-Induced.
- methods : Injections, Intraperitoneal, Microinjections.
- physiology : Circadian Rhythm, Motor Activity.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease.
- Animals, Disease Models, Animal, Female, Rats, Rats, Inbred Lew, Rats, Sprague-Dawley, Risk Factors, Rotation, Species Specificity, Time Factors, Treatment Outcome.
Abstract
Current treatments for Parkinson's disease rely on a dopamine replacement strategy and are reasonably effective, particularly in the early stages of the disease. However, chronic dopaminergic therapy is limited by the development of a range of side effects, including the onset of abnormal movements ('dyskinesia'). The neural mechanisms that underlie dyskinesia are far from clear but they have been associated with pulsatile stimulation of dopamine receptors, downstream changes in proteins and genes, and abnormalities in non-dopamine transmitter systems. However, there has been no pathophysiological explanation for the worsening motor symptoms in the afternoon and evening reported by Parkinsonian patients in long-term L-dopa therapy, and no direct relationship has been found with the pharmacokinetics of the drug. Moreover, there continues to be a debate about whether the development of dyskinesias in patients is dependent upon the duration of L-dopa treatment or on the degree of denervation/advanced stage of the disease, both factors that are difficult to resolve experimentally in the human disease. The objective of this study was to characterise, in an animal model, factors that predispose some individuals to develop dyskinesia after a prolonged treatment with L-dopa, whereas others continue to exhibit symptom alleviation without the side effects. We report that none of the parameters studied--genetic variation within and between strains, delay of treatment onset after lesion, or time of day of the drug treatment--were found to influence directly the formation of dyskinesias after L-dopa treatment. We conclude that a complex combination of individual factors are likely to interact to regulate the onset and development of abnormal movements in some animals but not others.
DOI: 10.1016/j.brainresbull.2008.11.007
PubMed: 19070653
Affiliations:
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However, chronic dopaminergic therapy is limited by the development of a range of side effects, including the onset of abnormal movements ('dyskinesia'). The neural mechanisms that underlie dyskinesia are far from clear but they have been associated with pulsatile stimulation of dopamine receptors, downstream changes in proteins and genes, and abnormalities in non-dopamine transmitter systems. However, there has been no pathophysiological explanation for the worsening motor symptoms in the afternoon and evening reported by Parkinsonian patients in long-term L-dopa therapy, and no direct relationship has been found with the pharmacokinetics of the drug. Moreover, there continues to be a debate about whether the development of dyskinesias in patients is dependent upon the duration of L-dopa treatment or on the degree of denervation/advanced stage of the disease, both factors that are difficult to resolve experimentally in the human disease. The objective of this study was to characterise, in an animal model, factors that predispose some individuals to develop dyskinesia after a prolonged treatment with L-dopa, whereas others continue to exhibit symptom alleviation without the side effects. We report that none of the parameters studied--genetic variation within and between strains, delay of treatment onset after lesion, or time of day of the drug treatment--were found to influence directly the formation of dyskinesias after L-dopa treatment. We conclude that a complex combination of individual factors are likely to interact to regulate the onset and development of abnormal movements in some animals but not others.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19070653</PMID><DateCreated><Year>2009</Year><Month>01</Month><Day>26</Day></DateCreated><DateCompleted><Year>2009</Year><Month>03</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2747</ISSN><JournalIssue CitedMedium="Internet"><Volume>78</Volume><Issue>4-5</Issue><PubDate><Year>2009</Year><Month>Mar</Month><Day>16</Day></PubDate></JournalIssue><Title>Brain research bulletin</Title><ISOAbbreviation>Brain Res. 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However, there has been no pathophysiological explanation for the worsening motor symptoms in the afternoon and evening reported by Parkinsonian patients in long-term L-dopa therapy, and no direct relationship has been found with the pharmacokinetics of the drug. Moreover, there continues to be a debate about whether the development of dyskinesias in patients is dependent upon the duration of L-dopa treatment or on the degree of denervation/advanced stage of the disease, both factors that are difficult to resolve experimentally in the human disease. The objective of this study was to characterise, in an animal model, factors that predispose some individuals to develop dyskinesia after a prolonged treatment with L-dopa, whereas others continue to exhibit symptom alleviation without the side effects. We report that none of the parameters studied--genetic variation within and between strains, delay of treatment onset after lesion, or time of day of the drug treatment--were found to influence directly the formation of dyskinesias after L-dopa treatment. We conclude that a complex combination of individual factors are likely to interact to regulate the onset and development of abnormal movements in some animals but not others.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Monville</LastName><ForeName>Christelle</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>INSERM/UEVE UMR861-ISTEM, AFM, 5, rue Henri Desbruères, 91030 Evry, France. cmonville@istem.genethon.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Torres</LastName><ForeName>Eduardo M</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Pekarik</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Lane</LastName><ForeName>Emma L</ForeName><Initials>EL</Initials></Author><Author ValidYN="Y"><LastName>Dunnett</LastName><ForeName>Stephen B</ForeName><Initials>SB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G-0501</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G0500794</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Brain Res Bull</MedlineTA><NlmUniqueID>7605818</NlmUniqueID><ISSNLinking>0361-9230</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013565">Sympatholytics</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002940" MajorTopicYN="N">Circadian Rhythm</DescriptorName><QualifierName UI="Q000502" 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MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008845" MajorTopicYN="N">Microinjections</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016627" MajorTopicYN="N">Oxidopamine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011917" MajorTopicYN="N">Rats, Inbred Lew</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012399" MajorTopicYN="N">Rotation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013045" MajorTopicYN="N">Species Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013565" MajorTopicYN="N">Sympatholytics</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2008</Year><Month>08</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2008</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2008</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>12</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>12</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>3</Month><Day>7</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19070653</ArticleId><ArticleId IdType="pii">S0361-9230(08)00396-1</ArticleId><ArticleId IdType="doi">10.1016/j.brainresbull.2008.11.007</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Evry</li></settlement></list><tree><noCountry><name sortKey="Dunnett, Stephen B" sort="Dunnett, Stephen B" uniqKey="Dunnett S" first="Stephen B" last="Dunnett">Stephen B. Dunnett</name><name sortKey="Lane, Emma L" sort="Lane, Emma L" uniqKey="Lane E" first="Emma L" last="Lane">Emma L. Lane</name><name sortKey="Pekarik, Vladimir" sort="Pekarik, Vladimir" uniqKey="Pekarik V" first="Vladimir" last="Pekarik">Vladimir Pekarik</name><name sortKey="Torres, Eduardo M" sort="Torres, Eduardo M" uniqKey="Torres E" first="Eduardo M" last="Torres">Eduardo M. Torres</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Monville, Christelle" sort="Monville, Christelle" uniqKey="Monville C" first="Christelle" last="Monville">Christelle Monville</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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