Selective blockade of D3 dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate
Identifieur interne : 000948 ( PascalFrancis/Corpus ); précédent : 000947; suivant : 000949Selective blockade of D3 dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate
Auteurs : M. A. Silverdale ; S. L. Nicholson ; P. Ravenscroft ; A. R. Crossman ; M. J. Millan ; J. M. BrotchieSource :
- Experimental neurology : (Print) [ 0014-4886 ] ; 2004.
Descripteurs français
- Pascal (Inist)
- Parkinson maladie, Récepteur dopaminergique D3, Ropinirole, Dyskinésie, Lévodopa, Primates, Antagoniste dopamine, Traitement, Sélectivité, Etude comparative, Récepteur dopaminergique D2, Dose faible, Récepteur dopaminergique, Stimulant dopaminergique, Conduite à tenir, Homme, Dopamine, Noyau gris central, Contrôle moteur.
English descriptors
- KwdEn :
Abstract
To date, the lack of highly selective antagonists at the dopamine D3receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D3 versus D2 receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D3-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses. S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D3 receptor stimulation. Indeed, stimulation of D3 receptors may be detrimental to the anti-parkinsonian properties of D2/D3 agonists. Selectivity for stimulation of D2, over D3, receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.
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Format Inist (serveur)
| NO : | PASCAL 05-0003811 INIST |
|---|---|
| ET : | Selective blockade of D3 dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate |
| AU : | SILVERDALE (M. A.); NICHOLSON (S. L.); RAVENSCROFT (P.); CROSSMAN (A. R.); MILLAN (M. J.); BROTCHIE (J. M.) |
| AF : | Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road/Manchester M13 9PT/Royaume-Uni (1 aut., 2 aut., 3 aut., 4 aut.); Department of Neurology, Hope Hospital/Salford M6 8HD/Royaume-Uni (1 aut.); Motac Neuroscience Ltd., Williams House/Manchester M15 6SE/Royaume-Uni (3 aut., 4 aut.); Department of Psychopharmacology, Institut de Recherches Servier, Centre de Recherches de Croissy/78290 Croissy-sur-Seine/France (5 aut.); Toronto Western Research Institute, University Health Network, Toronto Western Hospital/Toronto, Ontario, M5T 2S8/Canada (6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Experimental neurology : (Print); ISSN 0014-4886; Coden EXNEAC; Etats-Unis; Da. 2004; Vol. 188; No. 1; Pp. 128-138; Bibl. 2 p.1/4 |
| LA : | Anglais |
| EA : | To date, the lack of highly selective antagonists at the dopamine D3receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D3 versus D2 receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D3-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses. S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D3 receptor stimulation. Indeed, stimulation of D3 receptors may be detrimental to the anti-parkinsonian properties of D2/D3 agonists. Selectivity for stimulation of D2, over D3, receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia. |
| CC : | 002B02U01; 002B02B06 |
| FD : | Parkinson maladie; Récepteur dopaminergique D3; Ropinirole; Dyskinésie; Lévodopa; Primates; Antagoniste dopamine; Traitement; Sélectivité; Etude comparative; Récepteur dopaminergique D2; Dose faible; Récepteur dopaminergique; Stimulant dopaminergique; Conduite à tenir; Homme; Dopamine; Noyau gris central; Contrôle moteur |
| FG : | Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Antiparkinsonien; Mouvement involontaire; Trouble neurologique; Catécholamine; Neurotransmetteur; Système nerveux central |
| ED : | Parkinson disease; D3 Dopamine receptor; Ropinirole; Dyskinesia; Levodopa; Primates; Dopamine antagonist; Treatment; Selectivity; Comparative study; D2 Dopamine receptor; Low dose; Dopamine receptor; Dopamine agonist; Clinical management; Human; Dopamine; Basal ganglion; Motor control |
| EG : | Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Antiparkinson agent; Involuntary movement; Neurological disorder; Catecholamine; Neurotransmitter; Central nervous system |
| SD : | Parkinson enfermedad; Receptor dopaminérgico D3; Ropinirol; Disquinesia; Levodopa; Primates; Antagonista dopamina; Tratamiento; Selectividad; Estudio comparativo; Receptor dopaminérgico D2; Dosis débil; Receptor dopaminérgico; Estimulante dopaminérgico; Actitud médica; Hombre; Dopamina; Núcleo basal; Control motor |
| LO : | INIST-9181.354000122318750130 |
| ID : | 05-0003811 |
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Brotchie</name><affiliation><inist:fA14 i1="05"><s1>Toronto Western Research Institute, University Health Network, Toronto Western Hospital</s1><s2>Toronto, Ontario, M5T 2S8</s2><s3>CAN</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">05-0003811</idno><date when="2004">2004</date><idno type="stanalyst">PASCAL 05-0003811 INIST</idno><idno type="RBID">Pascal:05-0003811</idno><idno type="wicri:Area/PascalFrancis/Corpus">000948</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Selective blockade of D<sub>3</sub> dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate</title><author><name sortKey="Silverdale, M A" sort="Silverdale, M A" uniqKey="Silverdale M" first="M. A." last="Silverdale">M. A. Silverdale</name><affiliation><inist:fA14 i1="01"><s1>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road</s1><s2>Manchester M13 9PT</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Hope Hospital</s1><s2>Salford M6 8HD</s2><s3>GBR</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Nicholson, S L" sort="Nicholson, S L" uniqKey="Nicholson S" first="S. L." last="Nicholson">S. L. Nicholson</name><affiliation><inist:fA14 i1="01"><s1>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road</s1><s2>Manchester M13 9PT</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ravenscroft, P" sort="Ravenscroft, P" uniqKey="Ravenscroft P" first="P." last="Ravenscroft">P. Ravenscroft</name><affiliation><inist:fA14 i1="01"><s1>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road</s1><s2>Manchester M13 9PT</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Motac Neuroscience Ltd., Williams House</s1><s2>Manchester M15 6SE</s2><s3>GBR</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Crossman, A R" sort="Crossman, A R" uniqKey="Crossman A" first="A. R." last="Crossman">A. R. Crossman</name><affiliation><inist:fA14 i1="01"><s1>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road</s1><s2>Manchester M13 9PT</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Motac Neuroscience Ltd., Williams House</s1><s2>Manchester M15 6SE</s2><s3>GBR</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Millan, M J" sort="Millan, M J" uniqKey="Millan M" first="M. J." last="Millan">M. J. Millan</name><affiliation><inist:fA14 i1="04"><s1>Department of Psychopharmacology, Institut de Recherches Servier, Centre de Recherches de Croissy</s1><s2>78290 Croissy-sur-Seine</s2><s3>FRA</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Brotchie, J M" sort="Brotchie, J M" uniqKey="Brotchie J" first="J. M." last="Brotchie">J. M. Brotchie</name><affiliation><inist:fA14 i1="05"><s1>Toronto Western Research Institute, University Health Network, Toronto Western Hospital</s1><s2>Toronto, Ontario, M5T 2S8</s2><s3>CAN</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Experimental neurology : (Print)</title><title level="j" type="abbreviated">Exp. neurol. : (Print)</title><idno type="ISSN">0014-4886</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Experimental neurology : (Print)</title><title level="j" type="abbreviated">Exp. neurol. : (Print)</title><idno type="ISSN">0014-4886</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term><term>Clinical management</term><term>Comparative study</term><term>D2 Dopamine receptor</term><term>D3 Dopamine receptor</term><term>Dopamine</term><term>Dopamine agonist</term><term>Dopamine antagonist</term><term>Dopamine receptor</term><term>Dyskinesia</term><term>Human</term><term>Levodopa</term><term>Low dose</term><term>Motor control</term><term>Parkinson disease</term><term>Primates</term><term>Ropinirole</term><term>Selectivity</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Récepteur dopaminergique D3</term><term>Ropinirole</term><term>Dyskinésie</term><term>Lévodopa</term><term>Primates</term><term>Antagoniste dopamine</term><term>Traitement</term><term>Sélectivité</term><term>Etude comparative</term><term>Récepteur dopaminergique D2</term><term>Dose faible</term><term>Récepteur dopaminergique</term><term>Stimulant dopaminergique</term><term>Conduite à tenir</term><term>Homme</term><term>Dopamine</term><term>Noyau gris central</term><term>Contrôle moteur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To date, the lack of highly selective antagonists at the dopamine D<sub>3</sub>receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D<sub>3</sub> versus D<sub>2</sub> receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D<sub>3</sub>-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses. S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D<sub>3</sub> receptor stimulation. Indeed, stimulation of D<sub>3</sub> receptors may be detrimental to the anti-parkinsonian properties of D<sub>2</sub>/D<sub>3</sub> agonists. Selectivity for stimulation of D<sub>2</sub>, over D<sub>3</sub>, receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0014-4886</s0></fA01><fA02 i1="01"><s0>EXNEAC</s0></fA02><fA03 i2="1"><s0>Exp. neurol. : (Print)</s0></fA03><fA05><s2>188</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Selective blockade of D<sub>3</sub> dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate</s1></fA08><fA11 i1="01" i2="1"><s1>SILVERDALE (M. A.)</s1></fA11><fA11 i1="02" i2="1"><s1>NICHOLSON (S. 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M.)</s1></fA11><fA14 i1="01"><s1>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road</s1><s2>Manchester M13 9PT</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Neurology, Hope Hospital</s1><s2>Salford M6 8HD</s2><s3>GBR</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>Motac Neuroscience Ltd., Williams House</s1><s2>Manchester M15 6SE</s2><s3>GBR</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Psychopharmacology, Institut de Recherches Servier, Centre de Recherches de Croissy</s1><s2>78290 Croissy-sur-Seine</s2><s3>FRA</s3><sZ>5 aut.</sZ></fA14><fA14 i1="05"><s1>Toronto Western Research Institute, University Health Network, Toronto Western Hospital</s1><s2>Toronto, Ontario, M5T 2S8</s2><s3>CAN</s3><sZ>6 aut.</sZ></fA14><fA20><s1>128-138</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>9181</s2><s5>354000122318750130</s5></fA43><fA44><s0>0000</s0><s1>© 2005 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>2 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>05-0003811</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Experimental neurology : (Print)</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>To date, the lack of highly selective antagonists at the dopamine D<sub>3</sub>receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D<sub>3</sub> versus D<sub>2</sub> receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D<sub>3</sub>-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses. S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D<sub>3</sub> receptor stimulation. Indeed, stimulation of D<sub>3</sub> receptors may be detrimental to the anti-parkinsonian properties of D<sub>2</sub>/D<sub>3</sub> agonists. Selectivity for stimulation of D<sub>2</sub>, over D<sub>3</sub>, receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.</s0></fC01><fC02 i1="01" i2="X"><s0>002B02U01</s0></fC02><fC02 i1="02" i2="X"><s0>002B02B06</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Récepteur dopaminergique D3</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>D3 Dopamine receptor</s0><s5>02</s5><s6>«D3» Dopamine receptor</s6></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Receptor dopaminérgico D3</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Ropinirole</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" 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i2="X" l="SPA"><s0>Antagonista dopamina</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Traitement</s0><s5>09</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Treatment</s0><s5>09</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Tratamiento</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Sélectivité</s0><s5>11</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Selectivity</s0><s5>11</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Selectividad</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Etude comparative</s0><s5>12</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Comparative study</s0><s5>12</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Estudio comparativo</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Récepteur dopaminergique D2</s0><s5>14</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>D2 Dopamine receptor</s0><s5>14</s5><s6>«D2» Dopamine receptor</s6></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Receptor dopaminérgico D2</s0><s5>14</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Dose faible</s0><s5>15</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Low dose</s0><s5>15</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Dosis débil</s0><s5>15</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Récepteur dopaminergique</s0><s5>17</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Dopamine receptor</s0><s5>17</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Receptor dopaminérgico</s0><s5>17</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Stimulant dopaminergique</s0><s5>18</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Dopamine agonist</s0><s5>18</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Estimulante dopaminérgico</s0><s5>18</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Conduite à tenir</s0><s5>19</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Clinical management</s0><s5>19</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Actitud médica</s0><s5>19</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="16" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="16" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC03 i1="17" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>21</s5></fC03><fC03 i1="17" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>21</s5></fC03><fC03 i1="17" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>21</s5></fC03><fC03 i1="18" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>22</s5></fC03><fC03 i1="18" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>22</s5></fC03><fC03 i1="18" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>22</s5></fC03><fC03 i1="19" i2="X" l="FRE"><s0>Contrôle moteur</s0><s5>25</s5></fC03><fC03 i1="19" i2="X" l="ENG"><s0>Motor control</s0><s5>25</s5></fC03><fC03 i1="19" i2="X" l="SPA"><s0>Control motor</s0><s5>25</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>38</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>39</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>40</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>41</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>41</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>41</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Antiparkinsonien</s0><s5>42</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Antiparkinson agent</s0><s5>42</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Antiparkinsoniano</s0><s5>42</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Mouvement involontaire</s0><s5>43</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Involuntary movement</s0><s5>43</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Movimiento involuntario</s0><s5>43</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>45</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>45</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>45</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Catécholamine</s0><s5>46</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Catecholamine</s0><s5>46</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Catecolamina</s0><s5>46</s5></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>47</s5></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Neurotransmitter</s0><s5>47</s5></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Neurotransmisor</s0><s5>47</s5></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>48</s5></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Central nervous system</s0><s5>48</s5></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>48</s5></fC07><fN21><s1>004</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 05-0003811 INIST</NO><ET>Selective blockade of D<sub>3</sub> dopamine receptors enhances the anti-parkinsonian properties of ropinirole and levodopa in the MPTP-lesioned primate</ET><AU>SILVERDALE (M. A.); NICHOLSON (S. L.); RAVENSCROFT (P.); CROSSMAN (A. R.); MILLAN (M. J.); BROTCHIE (J. M.)</AU><AF>Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road/Manchester M13 9PT/Royaume-Uni (1 aut., 2 aut., 3 aut., 4 aut.); Department of Neurology, Hope Hospital/Salford M6 8HD/Royaume-Uni (1 aut.); Motac Neuroscience Ltd., Williams House/Manchester M15 6SE/Royaume-Uni (3 aut., 4 aut.); Department of Psychopharmacology, Institut de Recherches Servier, Centre de Recherches de Croissy/78290 Croissy-sur-Seine/France (5 aut.); Toronto Western Research Institute, University Health Network, Toronto Western Hospital/Toronto, Ontario, M5T 2S8/Canada (6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Experimental neurology : (Print); ISSN 0014-4886; Coden EXNEAC; Etats-Unis; Da. 2004; Vol. 188; No. 1; Pp. 128-138; Bibl. 2 p.1/4</SO><LA>Anglais</LA><EA>To date, the lack of highly selective antagonists at the dopamine D<sub>3</sub>receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D<sub>3</sub> versus D<sub>2</sub> receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D<sub>3</sub>-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses. S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D<sub>3</sub> receptor stimulation. Indeed, stimulation of D<sub>3</sub> receptors may be detrimental to the anti-parkinsonian properties of D<sub>2</sub>/D<sub>3</sub> agonists. Selectivity for stimulation of D<sub>2</sub>, over D<sub>3</sub>, receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.</EA><CC>002B02U01; 002B02B06</CC><FD>Parkinson maladie; Récepteur dopaminergique D3; Ropinirole; Dyskinésie; Lévodopa; Primates; Antagoniste dopamine; Traitement; Sélectivité; Etude comparative; Récepteur dopaminergique D2; Dose faible; Récepteur dopaminergique; Stimulant dopaminergique; Conduite à tenir; Homme; Dopamine; Noyau gris central; Contrôle moteur</FD><FG>Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Antiparkinsonien; Mouvement involontaire; Trouble neurologique; Catécholamine; Neurotransmetteur; Système nerveux central</FG><ED>Parkinson disease; D3 Dopamine receptor; Ropinirole; Dyskinesia; Levodopa; Primates; Dopamine antagonist; Treatment; Selectivity; Comparative study; D2 Dopamine receptor; Low dose; Dopamine receptor; Dopamine agonist; Clinical management; Human; Dopamine; Basal ganglion; Motor control</ED><EG>Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Antiparkinson agent; Involuntary movement; Neurological disorder; Catecholamine; Neurotransmitter; Central nervous system</EG><SD>Parkinson enfermedad; Receptor dopaminérgico D3; Ropinirol; Disquinesia; Levodopa; Primates; Antagonista dopamina; Tratamiento; Selectividad; Estudio comparativo; Receptor dopaminérgico D2; Dosis débil; Receptor dopaminérgico; Estimulante dopaminérgico; Actitud médica; Hombre; Dopamina; Núcleo basal; Control motor</SD><LO>INIST-9181.354000122318750130</LO><ID>05-0003811</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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