Movement Disorders (revue)

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Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets

Identifieur interne : 003018 ( Main/Exploration ); précédent : 003017; suivant : 003019

Antiparkinsonian activity of L‐propyl‐L‐leucyl‐glycinamide or melanocyte‐inhibiting factor in MPTP‐treated common marmosets

Auteurs : Regina Katzenschlager [Royaume-Uni, Autriche] ; Michael J. Jackson [Royaume-Uni] ; Sarah Rose [Royaume-Uni] ; Kim Stockwell [Royaume-Uni] ; Kayhan A. Tayarani-Binazir [Royaume-Uni] ; Mohammed Zubair [Royaume-Uni] ; Lance A. Smith [Royaume-Uni] ; Peter Jenner [Royaume-Uni] ; Andrew Lees (neurologue) [Royaume-Uni]

Source :

RBID : ISTEX:3A0D5F157B0A593D17D43EB7E889F5189630C0AD

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English descriptors

Abstract

The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society

Url:
DOI: 10.1002/mds.21256


Affiliations:


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<term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term>
<term>Administration, Oral</term>
<term>Animals</term>
<term>Antiparkinson Agents (administration & dosage)</term>
<term>Antiparkinson Agents (toxicity)</term>
<term>Benserazide (administration & dosage)</term>
<term>Benserazide (toxicity)</term>
<term>Callithrix</term>
<term>Dose-Response Relationship, Drug</term>
<term>Drug Therapy, Combination</term>
<term>Dyskinesia</term>
<term>Female</term>
<term>Infusions, Intravenous</term>
<term>Levodopa (administration & dosage)</term>
<term>Levodopa (toxicity)</term>
<term>Locomotion (drug effects)</term>
<term>MSH Release-Inhibiting Hormone (administration & dosage)</term>
<term>MSH Release-Inhibiting Hormone (toxicity)</term>
<term>Male</term>
<term>Motor Activity (drug effects)</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
<term>Parkinson's disease</term>
<term>Parkinsonian Disorders (drug therapy)</term>
<term>Treatment</term>
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<term>Dyskinésie</term>
<term>Parkinson maladie</term>
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<div type="abstract" xml:lang="en">The neuropeptide melanocyte‐inhibiting factor (MIF) or L‐propyl‐L‐leucyl‐glycinamide (PLG) has been reported in some studies to improve the motor signs of Parkinson's disease (PD) and in rodent models of PD. In this study of oral and intravenous MIF in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐lesioned marmosets, a wide range of doses of MIF administered alone (0.25, 1, 2, 5, 10, 20 mg/kg orally) did not increase locomotor activity, relieve motor disability, or induce dyskinesias. When MIF (1.0 and 5.0 mg/kg orally or 10 and 20 mg/kg intravenously) was administered concomitantly with levodopa/benserazide, no significant differences in motor function or dyskinesias were observed compared with levodopa/benserazide alone. The results of this first study of MIF in the marmoset MPTP model provide no encouragement for the reinvestigation of MIF in the clinical management of the motor signs of PD. © 2007 Movement Disorder Society</div>
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