Stimulation of cannabinoid receptors reduces levodopa‐induced dyskinesia in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Identifieur interne : 004280 ( Main/Exploration ); précédent : 004279; suivant : 004281Stimulation of cannabinoid receptors reduces levodopa‐induced dyskinesia in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Auteurs : Susan H. Fox [Royaume-Uni] ; Brian Henry [Royaume-Uni] ; Michael Hill [Royaume-Uni] ; Alan Crossman [Royaume-Uni] ; Jonathan Brotchie [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-11.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Agonist, Animal, Animal model, Animals, Antiparkinson Agents (toxicity), Antiparkinson agent, Benserazide (toxicity), Callithrix, Cannabinoid receptor, Chemotherapy, Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Dose-Response Relationship, Drug, Dronabinol (analogs & derivatives), Dronabinol (pharmacology), Drug Combinations, Drug Therapy, Combination, Dyskinesia, Dyskinesia, Drug-Induced (physiopathology), Female, Globus Pallidus (drug effects), Globus Pallidus (physiopathology), Levodopa, Levodopa (toxicity), MPTP, Male, Monkey, Motor Skills (drug effects), Nabilone, Parkinson disease, Parkinson's disease, Parkinsonian Disorders (physiopathology), Receptors, Cannabinoid, Receptors, Drug (drug effects), Receptors, Drug (physiology), Treatment, cannabinoid, dyskinesia, gamma-Aminobutyric Acid (metabolism), nabilone.
- MESH :
- chemical , analogs & derivatives : Dronabinol.
- chemical , drug effects : Receptors, Drug.
- chemical , metabolism : gamma-Aminobutyric Acid.
- chemical , pharmacology : Dronabinol.
- chemical , physiology : Receptors, Drug.
- chemical , toxicity : Antiparkinson Agents, Benserazide, Levodopa.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Drug Combinations, Receptors, Cannabinoid.
- drug effects : Corpus Striatum, Globus Pallidus, Motor Skills.
- physiopathology : Corpus Striatum, Dyskinesia, Drug-Induced, Globus Pallidus, Parkinsonian Disorders.
- Animals, Callithrix, Dose-Response Relationship, Drug, Drug Therapy, Combination, Female, Male.
Abstract
Long‐term treatment with levodopa in Parkinson's disease results in the development of motor fluctuations, including reduced duration of antiparkinsonian action and involuntary movements, i.e., levodopa‐induced dyskinesia. Cannabinoid receptors are concentrated in the basal ganglia, and stimulation of cannabinoid receptors can increase γ‐aminobutyric acid transmission in the lateral segment of globus pallidus and reduce glutamate release in the striatum. We thus tested the hypothesis that the cannabinoid receptor agonist nabilone (0.01, 0.03, and 0.10 mg/kg) would alleviate levodopa‐induced dyskinesia in the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine hydrochloride (MPTP) ‐lesioned marmoset model of Parkinson's disease. Coadministration of nabilone (0.1 mg/kg) with levodopa was associated with significantly less total dyskinesia (dyskinesia score, 12; range, 6–17; primate dyskinesia rating scale) than levodopa alone (22; range, 14–23; P < 0.05). This effect was more marked during the onset period (0–20 minutes post levodopa). There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of nabilone used (0.03 mg/kg) increased the duration of antiparkinsonian action of levodopa by 76%. Thus, cannabinoid receptor agonists may be useful in the treatment of motor complications in Parkinson's disease. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10289
Affiliations:
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Le document en format XML
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<term>Animal</term>
<term>Animal model</term>
<term>Animals</term>
<term>Antiparkinson Agents (toxicity)</term>
<term>Antiparkinson agent</term>
<term>Benserazide (toxicity)</term>
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<term>Cannabinoid receptor</term>
<term>Chemotherapy</term>
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<term>Corpus Striatum (physiopathology)</term>
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<term>Dronabinol (pharmacology)</term>
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<term>Female</term>
<term>Globus Pallidus (drug effects)</term>
<term>Globus Pallidus (physiopathology)</term>
<term>Levodopa</term>
<term>Levodopa (toxicity)</term>
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<front><div type="abstract" xml:lang="en">Long‐term treatment with levodopa in Parkinson's disease results in the development of motor fluctuations, including reduced duration of antiparkinsonian action and involuntary movements, i.e., levodopa‐induced dyskinesia. Cannabinoid receptors are concentrated in the basal ganglia, and stimulation of cannabinoid receptors can increase γ‐aminobutyric acid transmission in the lateral segment of globus pallidus and reduce glutamate release in the striatum. We thus tested the hypothesis that the cannabinoid receptor agonist nabilone (0.01, 0.03, and 0.10 mg/kg) would alleviate levodopa‐induced dyskinesia in the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine hydrochloride (MPTP) ‐lesioned marmoset model of Parkinson's disease. Coadministration of nabilone (0.1 mg/kg) with levodopa was associated with significantly less total dyskinesia (dyskinesia score, 12; range, 6–17; primate dyskinesia rating scale) than levodopa alone (22; range, 14–23; P < 0.05). This effect was more marked during the onset period (0–20 minutes post levodopa). There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of nabilone used (0.03 mg/kg) increased the duration of antiparkinsonian action of levodopa by 76%. Thus, cannabinoid receptor agonists may be useful in the treatment of motor complications in Parkinson's disease. © 2002 Movement Disorder Society</div>
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