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.