Effect of chronic treatment with (+)-PHNO, a D2 agonist in MPTP-treated monkeys
Identifieur interne : 004526 ( Main/Exploration ); précédent : 004525; suivant : 004527Effect of chronic treatment with (+)-PHNO, a D2 agonist in MPTP-treated monkeys
Auteurs : Baltazar Gomez-Mancilla [Canada] ; Paul J. Bédard [Canada]Source :
- Experimental Neurology [ 0014-4886 ] ; 1992.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animal, Animals, Antiparkinson Agents (pharmacology), Antiparkinson agent, Chemotherapy, D2 Dopamine receptor, Dopamine Agents (pharmacology), Dopamine agonist, Experimental disease, Female, Indoles (pharmacology), MPTP Poisoning, Macaca fascicularis, Motor Activity (drug effects), Oxazines (pharmacology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Parkinson disease, Pathophysiology, Phenanthridines (pharmacology), Receptors, Dopamine (drug effects), Receptors, Dopamine (physiology), Receptors, Dopamine D1, Receptors, Dopamine D2, Treatment.
- MESH :
- chemical , drug effects : Receptors, Dopamine.
- chemical , pharmacology : Antiparkinson Agents, Dopamine Agents, Indoles, Oxazines, Phenanthridines.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Motor Activity.
- chemical , physiology : Receptors, Dopamine.
- physiopathology : Parkinson Disease, Secondary.
- Animals, Female, MPTP Poisoning, Macaca fascicularis, Receptors, Dopamine D1, Receptors, Dopamine D2.
Abstract
A group of four drug naive Macaca fascicularis were rendered parkinsonian with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and then treated chronically with (+)-PHNO, a potent D2 agonist. After several days, dyskinesia appeared in all animals. At this point, the daily dose of (+)-PHNO was replaced by a dose of the D1 agonist CY 208–243. The substitution by CY 208–243 reproduced the same dyskinesia observed with (+)-PHNO. The administration of the DA synthesis inhibitor AMPT (α-methyl-p-tyrosine methyl ester) blocked the dyskinetic and antiparkinsonian effect of (+)-PHNO, and those effects were reestablished by the addition of a subthreshold dose of CY 208–243. Our results show that a selective D2 agonist is capable of inducing dyskinesia and suggest some kind of cooperation between D1 and D2 receptors in the antiparkinsonian and dyskinetic effect produced by (+)-PHNO.
Url:
DOI: 10.1016/0014-4886(92)90125-A
Affiliations:
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Le document en format XML
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<term>Chemotherapy</term>
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<front><div type="abstract" xml:lang="en">A group of four drug naive Macaca fascicularis were rendered parkinsonian with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and then treated chronically with (+)-PHNO, a potent D2 agonist. After several days, dyskinesia appeared in all animals. At this point, the daily dose of (+)-PHNO was replaced by a dose of the D1 agonist CY 208–243. The substitution by CY 208–243 reproduced the same dyskinesia observed with (+)-PHNO. The administration of the DA synthesis inhibitor AMPT (α-methyl-p-tyrosine methyl ester) blocked the dyskinetic and antiparkinsonian effect of (+)-PHNO, and those effects were reestablished by the addition of a subthreshold dose of CY 208–243. Our results show that a selective D2 agonist is capable of inducing dyskinesia and suggest some kind of cooperation between D1 and D2 receptors in the antiparkinsonian and dyskinetic effect produced by (+)-PHNO.</div>
</front>
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