Sustained cabergoline treatment reverses levodopa-induced dyskinesias in parkinsonian monkeys
Identifieur interne : 000B53 ( PascalFrancis/Checkpoint ); précédent : 000B52; suivant : 000B54Sustained cabergoline treatment reverses levodopa-induced dyskinesias in parkinsonian monkeys
Auteurs : ABDALLAH HADJ TAHAR [Canada] ; Laurent Gregoire [Canada] ; Evelyne Bangassoro [Canada] ; Paul J. Bedard [Canada]Source :
- Clinical neuropharmacology [ 0362-5664 ] ; 2000.
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Abstract
The pathophysiology of L-Dopa-induced dyskinesias (LID), a common problem after long-term use of L-dopa in the treatment of Parkinson's disease (PD), is not completely understood. Oscillations in L-Dopa concentrations in the brain are believed to be responsible, at least in part, for their pathogenesis. This study was aimed at verifying whether chronic administration of cabergoline, a long-acting dopamine D2-like receptor agonist, can reverse established LID. Four MPTP-treated cynomolgus monkeys with long-standing and stable parkinsonian syndrome and reproducible dyskinesias to L-Dopa, were used in this study. We compared the antiparkinsonian and dyskinetic responses of L-Dopa methyl ester (62.5 mg and 125 mg), given with benserazide (50 mg) (L-Dopa/benserazide), administered before and after a 6-week period during which the animals were treated only by daily administration of cabergoline (doses ranging from 0.125 to 0.185 mg/kg, subcutaneous). During cabergoline treatment, the monkeys initially showed marked dyskinesias, which were reduced significantly after 4 weeks of treatment. However, there was no tolerance to its antiparkinsonian effect. L-Dopa/benserazide given 4 days after cabergoline withdrawal produced a significant antiparkinsonian effect, but dyskinesias were dramatically reduced compared to what had been seen before chronic cabergoline treatment. The duration of the L-Dopa response was not increased after chronic administration of cabergoline. Our data suggest that sustained dopamine D2 receptor stimulation could be of value when trying to reduce or to reverse LID in patients with fluctuating advanced PD.
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Bedard</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, School of Medicine and Neuroscience Research Unit, Laval University Research Center</s1><s2>Ste-Foy, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Ste-Foy, Québec</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Clinical neuropharmacology</title><title level="j" type="abbreviated">Clin. neuropharmacol.</title><idno type="ISSN">0362-5664</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Clinical neuropharmacology</title><title level="j" type="abbreviated">Clin. neuropharmacol.</title><idno type="ISSN">0362-5664</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Agonist</term><term>Animal</term><term>Antiparkinson agent</term><term>Biological activity</term><term>Cabergoline</term><term>Chemotherapy</term><term>D2 Dopamine receptor</term><term>Dopamine agonist</term><term>Dose activity relation</term><term>Dyskinesia</term><term>Ergot derivatives</term><term>Levodopa</term><term>Long term</term><term>Monkey</term><term>Parkinson disease</term><term>Subcutaneous administration</term><term>Toxicity</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Lévodopa</term><term>Antiparkinsonien</term><term>Parkinson maladie</term><term>Dyskinésie</term><term>Toxicité</term><term>Cabergoline</term><term>Stimulant dopaminergique</term><term>Récepteur dopaminergique D2</term><term>Agoniste</term><term>Traitement</term><term>Chimiothérapie</term><term>Activité biologique</term><term>Long terme</term><term>Relation dose réponse</term><term>Animal</term><term>Ergot dérivé</term><term>Singe</term><term>Voie souscutanée</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathophysiology of L-Dopa-induced dyskinesias (LID), a common problem after long-term use of L-dopa in the treatment of Parkinson's disease (PD), is not completely understood. Oscillations in L-Dopa concentrations in the brain are believed to be responsible, at least in part, for their pathogenesis. This study was aimed at verifying whether chronic administration of cabergoline, a long-acting dopamine D<sub>2</sub>-like receptor agonist, can reverse established LID. Four MPTP-treated cynomolgus monkeys with long-standing and stable parkinsonian syndrome and reproducible dyskinesias to L-Dopa, were used in this study. We compared the antiparkinsonian and dyskinetic responses of L-Dopa methyl ester (62.5 mg and 125 mg), given with benserazide (50 mg) (L-Dopa/benserazide), administered before and after a 6-week period during which the animals were treated only by daily administration of cabergoline (doses ranging from 0.125 to 0.185 mg/kg, subcutaneous). During cabergoline treatment, the monkeys initially showed marked dyskinesias, which were reduced significantly after 4 weeks of treatment. However, there was no tolerance to its antiparkinsonian effect. L-Dopa/benserazide given 4 days after cabergoline withdrawal produced a significant antiparkinsonian effect, but dyskinesias were dramatically reduced compared to what had been seen before chronic cabergoline treatment. The duration of the L-Dopa response was not increased after chronic administration of cabergoline. Our data suggest that sustained dopamine D<sub>2</sub> receptor stimulation could be of value when trying to reduce or to reverse LID in patients with fluctuating advanced PD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0362-5664</s0></fA01><fA02 i1="01"><s0>CLNEDB</s0></fA02><fA03 i2="1"><s0>Clin. neuropharmacol.</s0></fA03><fA05><s2>23</s2></fA05><fA06><s2>4</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Sustained cabergoline treatment reverses levodopa-induced dyskinesias in parkinsonian monkeys</s1></fA08><fA11 i1="01" i2="1"><s1>ABDALLAH HADJ TAHAR</s1></fA11><fA11 i1="02" i2="1"><s1>GREGOIRE (Laurent)</s1></fA11><fA11 i1="03" i2="1"><s1>BANGASSORO (Evelyne)</s1></fA11><fA11 i1="04" i2="1"><s1>BEDARD (Paul J.)</s1></fA11><fA14 i1="01"><s1>Department of Medicine, School of Medicine and Neuroscience Research Unit, Laval University Research Center</s1><s2>Ste-Foy, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></fA14><fA20><s1>195-202</s1></fA20><fA21><s1>2000</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>16720</s2><s5>354000091364260050</s5></fA43><fA44><s0>0000</s0><s1>© 2000 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>76 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>00-0500117</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Clinical neuropharmacology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>The pathophysiology of L-Dopa-induced dyskinesias (LID), a common problem after long-term use of L-dopa in the treatment of Parkinson's disease (PD), is not completely understood. Oscillations in L-Dopa concentrations in the brain are believed to be responsible, at least in part, for their pathogenesis. This study was aimed at verifying whether chronic administration of cabergoline, a long-acting dopamine D<sub>2</sub>-like receptor agonist, can reverse established LID. Four MPTP-treated cynomolgus monkeys with long-standing and stable parkinsonian syndrome and reproducible dyskinesias to L-Dopa, were used in this study. We compared the antiparkinsonian and dyskinetic responses of L-Dopa methyl ester (62.5 mg and 125 mg), given with benserazide (50 mg) (L-Dopa/benserazide), administered before and after a 6-week period during which the animals were treated only by daily administration of cabergoline (doses ranging from 0.125 to 0.185 mg/kg, subcutaneous). During cabergoline treatment, the monkeys initially showed marked dyskinesias, which were reduced significantly after 4 weeks of treatment. However, there was no tolerance to its antiparkinsonian effect. L-Dopa/benserazide given 4 days after cabergoline withdrawal produced a significant antiparkinsonian effect, but dyskinesias were dramatically reduced compared to what had been seen before chronic cabergoline treatment. The duration of the L-Dopa response was not increased after chronic administration of cabergoline. 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l="SPA"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>332</s1></fN21></pA></standard></inist><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Abdallah Hadj Tahar" sort="Abdallah Hadj Tahar" uniqKey="Abdallah Hadj Tahar" last="Abdallah Hadj Tahar">ABDALLAH HADJ TAHAR</name></noRegion><name sortKey="Bangassoro, Evelyne" sort="Bangassoro, Evelyne" uniqKey="Bangassoro E" first="Evelyne" last="Bangassoro">Evelyne Bangassoro</name><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bedard">Paul J. Bedard</name><name sortKey="Gregoire, Laurent" sort="Gregoire, Laurent" uniqKey="Gregoire L" first="Laurent" last="Gregoire">Laurent Gregoire</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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