The Selective Mu-Opioid Receptor Antagonist ADL5510 Reduces Levodopa-Induced Dyskinesia Without Affecting Antiparkinsonian Action in MPTP-Lesioned Macaque Model of Parkinson's Disease
Identifieur interne : 000305 ( PascalFrancis/Corpus ); précédent : 000304; suivant : 000306The Selective Mu-Opioid Receptor Antagonist ADL5510 Reduces Levodopa-Induced Dyskinesia Without Affecting Antiparkinsonian Action in MPTP-Lesioned Macaque Model of Parkinson's Disease
Auteurs : James B. Koprich ; Susan H. Fox ; Tom H. Johnston ; Allan Goodman ; Bertrand Le Bourdonnec ; Roland E. Dolle ; Robert N. Dehaven ; Diane L. Dehaven-Hudkins ; Patrick J. Little ; Jonathan M. BrotchieSource :
- Movement disorders [ 0885-3185 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
In Parkinson's disease (PD), dyskinesia develops following long-term treatment with 3,4-dihydroxyphenylalanine (L-dopa). Given the prominent role of the opioid system in basal ganglia function, non-selective opioid receptor antagonists have been tested for antidyskinetic efficacy in the clinic (naltrexone and naloxone), although without success. In the current study, ADL5510, a novel, orally active opioid antagonist with mu opioid receptor selectivity, was examined in L-dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) macaques. Antidyskinetic effects were compared with those of naltrexone. Parkinsonian monkeys with established L-dopa-induced dyskinesia (LID) received acute challenges with L-dopa (subcutaneously) in combination with either vehicle, ADL5510 (0.1, 1, 3 or 10 mg/kg by mouth), or naltrexone (1, 3, or 10 mg/kg subcutaneously). Following treatments, behavior was monitored for 6 hours. Parameters assessed were total activity, parkinsonism, and dyskinesia. ADL5510 (1, 3, and 10 mg/kg) reduced activity and LID (chorea and dystonia) without affecting the antiparkinsonian benefits of L-dopa. The antidyskinetic effect of ADL5510 showed a U-shaped dose-response. It was inactive at 0.1 mg/ kg, efficacious at 1 and 3 mg/kg (72% and 40% reductions, respectively), and then less effective at 10 mg/kg. The quality of ON time produced by L-dopa was improved, as indicated by a reduction in the percentage of ON time spent experiencing disabling dyskinesia (70% and 61 % reductions with 1 and 3 mg/kg, respectively, compared with L-dopa). Naltrexone, in contrast, did not alleviate LID or affect the antiparkinsonian actions of L-dopa. Mu-selective opioid antagonists have the potential to form the basis of novel antidyskinetic therapies for PD.
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Format Inist (serveur)
NO : | PASCAL 11-0321195 INIST |
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ET : | The Selective Mu-Opioid Receptor Antagonist ADL5510 Reduces Levodopa-Induced Dyskinesia Without Affecting Antiparkinsonian Action in MPTP-Lesioned Macaque Model of Parkinson's Disease |
AU : | KOPRICH (James B.); FOX (Susan H.); JOHNSTON (Tom H.); GOODMAN (Allan); LE BOURDONNEC (Bertrand); DOLLE (Roland E.); DEHAVEN (Robert N.); DEHAVEN-HUDKINS (Diane L.); LITTLE (Patrick J.); BROTCHIE (Jonathan M.) |
AF : | Toronto Western Research Institute, Toronto Western Hospital, University Health Network/Toronto, Ontario/Canada (1 aut., 3 aut., 10 aut.); Atuka Ltd./Toronto, Ontario/Canada (1 aut., 3 aut., 10 aut.); Division of Neurology, University of Toronto and Movement Disorders Clinic, Toronto Western Hospital, University Health Network/Toronto, Ontario/Canada (2 aut.); Adolor Corp./Exton, Pennsylvania/Etats-Unis (4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 7; Pp. 1225-1233; Bibl. 48 ref. |
LA : | Anglais |
EA : | In Parkinson's disease (PD), dyskinesia develops following long-term treatment with 3,4-dihydroxyphenylalanine (L-dopa). Given the prominent role of the opioid system in basal ganglia function, non-selective opioid receptor antagonists have been tested for antidyskinetic efficacy in the clinic (naltrexone and naloxone), although without success. In the current study, ADL5510, a novel, orally active opioid antagonist with mu opioid receptor selectivity, was examined in L-dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyri dine (MPTP) macaques. Antidyskinetic effects were compared with those of naltrexone. Parkinsonian monkeys with established L-dopa-induced dyskinesia (LID) received acute challenges with L-dopa (subcutaneously) in combination with either vehicle, ADL5510 (0.1, 1, 3 or 10 mg/kg by mouth), or naltrexone (1, 3, or 10 mg/kg subcutaneously). Following treatments, behavior was monitored for 6 hours. Parameters assessed were total activity, parkinsonism, and dyskinesia. ADL5510 (1, 3, and 10 mg/kg) reduced activity and LID (chorea and dystonia) without affecting the antiparkinsonian benefits of L-dopa. The antidyskinetic effect of ADL5510 showed a U-shaped dose-response. It was inactive at 0.1 mg/ kg, efficacious at 1 and 3 mg/kg (72% and 40% reductions, respectively), and then less effective at 10 mg/kg. The quality of ON time produced by L-dopa was improved, as indicated by a reduction in the percentage of ON time spent experiencing disabling dyskinesia (70% and 61 % reductions with 1 and 3 mg/kg, respectively, compared with L-dopa). Naltrexone, in contrast, did not alleviate LID or affect the antiparkinsonian actions of L-dopa. Mu-selective opioid antagonists have the potential to form the basis of novel antidyskinetic therapies for PD. |
CC : | 002B17; 002B17G |
FD : | Dyskinésie; Maladie de Parkinson; Pathologie du système nerveux; Récepteur opiacé; Lévodopa; Singe; Modèle; Homme |
FG : | Primates; Mammalia; Vertebrata; Syndrome extrapyramidal; Mouvement involontaire; Trouble neurologique; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Dyskinesia; Parkinson disease; Nervous system diseases; Opioid receptor; Levodopa; Monkey; Models; Human |
EG : | Primates; Mammalia; Vertebrata; Extrapyramidal syndrome; Involuntary movement; Neurological disorder; Cerebral disorder; Degenerative disease; Central nervous system disease |
SD : | Disquinesia; Parkinson enfermedad; Sistema nervioso patología; Receptor opiáceo; Levodopa; Mono; Modelo; Hombre |
LO : | INIST-20953.354000190480410060 |
ID : | 11-0321195 |
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Pascal:11-0321195Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">The Selective Mu-Opioid Receptor Antagonist ADL5510 Reduces Levodopa-Induced Dyskinesia Without Affecting Antiparkinsonian Action in MPTP-Lesioned Macaque Model of Parkinson's Disease</title>
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<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2011">2011</date>
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<seriesStmt><title level="j" type="main">Movement disorders</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dyskinesia</term>
<term>Human</term>
<term>Levodopa</term>
<term>Models</term>
<term>Monkey</term>
<term>Nervous system diseases</term>
<term>Opioid receptor</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dyskinésie</term>
<term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Récepteur opiacé</term>
<term>Lévodopa</term>
<term>Singe</term>
<term>Modèle</term>
<term>Homme</term>
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<front><div type="abstract" xml:lang="en">In Parkinson's disease (PD), dyskinesia develops following long-term treatment with 3,4-dihydroxyphenylalanine (<sub>L</sub>
-dopa). Given the prominent role of the opioid system in basal ganglia function, non-selective opioid receptor antagonists have been tested for antidyskinetic efficacy in the clinic (naltrexone and naloxone), although without success. In the current study, ADL5510, a novel, orally active opioid antagonist with mu opioid receptor selectivity, was examined in L-dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) macaques. Antidyskinetic effects were compared with those of naltrexone. Parkinsonian monkeys with established <sub>L</sub>
-dopa-induced dyskinesia (LID) received acute challenges with <sub>L</sub>
-dopa (subcutaneously) in combination with either vehicle, ADL5510 (0.1, 1, 3 or 10 mg/kg by mouth), or naltrexone (1, 3, or 10 mg/kg subcutaneously). Following treatments, behavior was monitored for 6 hours. Parameters assessed were total activity, parkinsonism, and dyskinesia. ADL5510 (1, 3, and 10 mg/kg) reduced activity and LID (chorea and dystonia) without affecting the antiparkinsonian benefits of <sub>L</sub>
-dopa. The antidyskinetic effect of ADL5510 showed a U-shaped dose-response. It was inactive at 0.1 mg/ kg, efficacious at 1 and 3 mg/kg (72% and 40% reductions, respectively), and then less effective at 10 mg/kg. The quality of ON time produced by <sub>L</sub>
-dopa was improved, as indicated by a reduction in the percentage of ON time spent experiencing disabling dyskinesia (70% and 61 % reductions with 1 and 3 mg/kg, respectively, compared with <sub>L</sub>
-dopa). Naltrexone, in contrast, did not alleviate LID or affect the antiparkinsonian actions of <sub>L</sub>
-dopa. Mu-selective opioid antagonists have the potential to form the basis of novel antidyskinetic therapies for PD.</div>
</front>
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<s3>CAN</s3>
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<sZ>3 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Atuka Ltd.</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Division of Neurology, University of Toronto and Movement Disorders Clinic, Toronto Western Hospital, University Health Network</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Adolor Corp.</s1>
<s2>Exton, Pennsylvania</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>1225-1233</s1>
</fA20>
<fA21><s1>2011</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000190480410060</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2011 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>48 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>11-0321195</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>In Parkinson's disease (PD), dyskinesia develops following long-term treatment with 3,4-dihydroxyphenylalanine (<sub>L</sub>
-dopa). Given the prominent role of the opioid system in basal ganglia function, non-selective opioid receptor antagonists have been tested for antidyskinetic efficacy in the clinic (naltrexone and naloxone), although without success. In the current study, ADL5510, a novel, orally active opioid antagonist with mu opioid receptor selectivity, was examined in L-dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) macaques. Antidyskinetic effects were compared with those of naltrexone. Parkinsonian monkeys with established <sub>L</sub>
-dopa-induced dyskinesia (LID) received acute challenges with <sub>L</sub>
-dopa (subcutaneously) in combination with either vehicle, ADL5510 (0.1, 1, 3 or 10 mg/kg by mouth), or naltrexone (1, 3, or 10 mg/kg subcutaneously). Following treatments, behavior was monitored for 6 hours. Parameters assessed were total activity, parkinsonism, and dyskinesia. ADL5510 (1, 3, and 10 mg/kg) reduced activity and LID (chorea and dystonia) without affecting the antiparkinsonian benefits of <sub>L</sub>
-dopa. The antidyskinetic effect of ADL5510 showed a U-shaped dose-response. It was inactive at 0.1 mg/ kg, efficacious at 1 and 3 mg/kg (72% and 40% reductions, respectively), and then less effective at 10 mg/kg. The quality of ON time produced by <sub>L</sub>
-dopa was improved, as indicated by a reduction in the percentage of ON time spent experiencing disabling dyskinesia (70% and 61 % reductions with 1 and 3 mg/kg, respectively, compared with <sub>L</sub>
-dopa). Naltrexone, in contrast, did not alleviate LID or affect the antiparkinsonian actions of <sub>L</sub>
-dopa. Mu-selective opioid antagonists have the potential to form the basis of novel antidyskinetic therapies for PD.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Dyskinésie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dyskinesia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Disquinesia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Récepteur opiacé</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Opioid receptor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Receptor opiáceo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lévodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Singe</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Monkey</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Mono</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Modèle</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Models</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Modelo</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Homme</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Human</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Hombre</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>43</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>43</s5>
</fC07>
<fN21><s1>220</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 11-0321195 INIST</NO>
<ET>The Selective Mu-Opioid Receptor Antagonist ADL5510 Reduces Levodopa-Induced Dyskinesia Without Affecting Antiparkinsonian Action in MPTP-Lesioned Macaque Model of Parkinson's Disease</ET>
<AU>KOPRICH (James B.); FOX (Susan H.); JOHNSTON (Tom H.); GOODMAN (Allan); LE BOURDONNEC (Bertrand); DOLLE (Roland E.); DEHAVEN (Robert N.); DEHAVEN-HUDKINS (Diane L.); LITTLE (Patrick J.); BROTCHIE (Jonathan M.)</AU>
<AF>Toronto Western Research Institute, Toronto Western Hospital, University Health Network/Toronto, Ontario/Canada (1 aut., 3 aut., 10 aut.); Atuka Ltd./Toronto, Ontario/Canada (1 aut., 3 aut., 10 aut.); Division of Neurology, University of Toronto and Movement Disorders Clinic, Toronto Western Hospital, University Health Network/Toronto, Ontario/Canada (2 aut.); Adolor Corp./Exton, Pennsylvania/Etats-Unis (4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 7; Pp. 1225-1233; Bibl. 48 ref.</SO>
<LA>Anglais</LA>
<EA>In Parkinson's disease (PD), dyskinesia develops following long-term treatment with 3,4-dihydroxyphenylalanine (<sub>L</sub>
-dopa). Given the prominent role of the opioid system in basal ganglia function, non-selective opioid receptor antagonists have been tested for antidyskinetic efficacy in the clinic (naltrexone and naloxone), although without success. In the current study, ADL5510, a novel, orally active opioid antagonist with mu opioid receptor selectivity, was examined in L-dopa-treated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyri dine (MPTP) macaques. Antidyskinetic effects were compared with those of naltrexone. Parkinsonian monkeys with established <sub>L</sub>
-dopa-induced dyskinesia (LID) received acute challenges with <sub>L</sub>
-dopa (subcutaneously) in combination with either vehicle, ADL5510 (0.1, 1, 3 or 10 mg/kg by mouth), or naltrexone (1, 3, or 10 mg/kg subcutaneously). Following treatments, behavior was monitored for 6 hours. Parameters assessed were total activity, parkinsonism, and dyskinesia. ADL5510 (1, 3, and 10 mg/kg) reduced activity and LID (chorea and dystonia) without affecting the antiparkinsonian benefits of <sub>L</sub>
-dopa. The antidyskinetic effect of ADL5510 showed a U-shaped dose-response. It was inactive at 0.1 mg/ kg, efficacious at 1 and 3 mg/kg (72% and 40% reductions, respectively), and then less effective at 10 mg/kg. The quality of ON time produced by <sub>L</sub>
-dopa was improved, as indicated by a reduction in the percentage of ON time spent experiencing disabling dyskinesia (70% and 61 % reductions with 1 and 3 mg/kg, respectively, compared with <sub>L</sub>
-dopa). Naltrexone, in contrast, did not alleviate LID or affect the antiparkinsonian actions of <sub>L</sub>
-dopa. Mu-selective opioid antagonists have the potential to form the basis of novel antidyskinetic therapies for PD.</EA>
<CC>002B17; 002B17G</CC>
<FD>Dyskinésie; Maladie de Parkinson; Pathologie du système nerveux; Récepteur opiacé; Lévodopa; Singe; Modèle; Homme</FD>
<FG>Primates; Mammalia; Vertebrata; Syndrome extrapyramidal; Mouvement involontaire; Trouble neurologique; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>Dyskinesia; Parkinson disease; Nervous system diseases; Opioid receptor; Levodopa; Monkey; Models; Human</ED>
<EG>Primates; Mammalia; Vertebrata; Extrapyramidal syndrome; Involuntary movement; Neurological disorder; Cerebral disorder; Degenerative disease; Central nervous system disease</EG>
<SD>Disquinesia; Parkinson enfermedad; Sistema nervioso patología; Receptor opiáceo; Levodopa; Mono; Modelo; Hombre</SD>
<LO>INIST-20953.354000190480410060</LO>
<ID>11-0321195</ID>
</server>
</inist>
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