The nociceptin/orphanin FQ (NOP) receptor antagonist J‐113397 enhances the effects of levodopa in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Identifieur interne : 003156 ( Main/Merge ); précédent : 003155; suivant : 003157The nociceptin/orphanin FQ (NOP) receptor antagonist J‐113397 enhances the effects of levodopa in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Auteurs : Naomi P. Visanji [Canada] ; Rob M. A. De Bie [Canada, Pays-Bas] ; Tom H. Johnston [Canada] ; Andrew C. Mccreary [Pays-Bas] ; Jonathan M. Brotchie [Canada] ; Susan H. Fox [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-10-15.
English descriptors
- KwdEn :
- Analysis of Variance, Animals, Antiparkinson Agents (therapeutic use), Benzimidazoles (therapeutic use), Callithrix, Disability Evaluation, Disease Models, Animal, Drug Synergism, Levodopa (therapeutic use), MPTP, MPTP Poisoning (drug therapy), Opioid Peptides (antagonists & inhibitors), Piperidines (therapeutic use), Time Factors, dyskinesia, levodopa, marmoset, nociceptin/orphanin FQ.
- MESH :
- chemical , antagonists & inhibitors : Opioid Peptides.
- chemical , therapeutic use : Antiparkinson Agents, Benzimidazoles, Levodopa, Piperidines.
- drug therapy : MPTP Poisoning.
- Analysis of Variance, Animals, Callithrix, Disability Evaluation, Disease Models, Animal, Drug Synergism, Time Factors.
Abstract
The anti‐parkinsonian and levodopa‐sparing potential of the nociceptin/orphanin FQ receptor (NOP) antagonist J‐113397 has been demonstrated in rodent models of Parkinson's disease. Here, we describe the levodopa‐sparing potential of J‐113397 in MPTP‐lesioned marmosets. Coadministration of J‐113397 (30 mg/kg) with a sub‐therapeutic dose of levodopa (12.5 mg/kg) produced an anti‐parkinsonian action equivalent to that of a therapeutic dose of levodopa. However, these effects were accompanied by an equivalent level of dyskinesia. The actions of NOP antagonists seen in rodents translate to nonhuman primates. However, the present study raises the possibility that these levodopa‐sparing benefits may be offset by a propensity to exacerbate dyskinesia. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22086
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<term>Benzimidazoles (therapeutic use)</term>
<term>Callithrix</term>
<term>Disability Evaluation</term>
<term>Disease Models, Animal</term>
<term>Drug Synergism</term>
<term>Levodopa (therapeutic use)</term>
<term>MPTP Poisoning (drug therapy)</term>
<term>Opioid Peptides (antagonists & inhibitors)</term>
<term>Piperidines (therapeutic use)</term>
<term>Time Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Opioid Peptides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Benzimidazoles</term>
<term>Levodopa</term>
<term>Piperidines</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>MPTP Poisoning</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term>
<term>Animals</term>
<term>Callithrix</term>
<term>Disability Evaluation</term>
<term>Disease Models, Animal</term>
<term>Drug Synergism</term>
<term>Time Factors</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The anti-parkinsonian and levodopa-sparing potential of the nociceptin/orphanin FQ receptor (NOP) antagonist J-113397 has been demonstrated in rodent models of Parkinson's disease. Here, we describe the levodopa-sparing potential of J-113397 in MPTP-lesioned marmosets. Coadministration of J-113397 (30 mg/kg) with a sub-therapeutic dose of levodopa (12.5 mg/kg) produced an anti-parkinsonian action equivalent to that of a therapeutic dose of levodopa. However, these effects were accompanied by an equivalent level of dyskinesia. The actions of NOP antagonists seen in rodents translate to nonhuman primates. However, the present study raises the possibility that these levodopa-sparing benefits may be offset by a propensity to exacerbate dyskinesia.</div>
</front>
</TEI>
</PubMed>
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