Easily definable dyskinetic syndromes have been produced by injection of L-DOPA, apomorphine, trivastal, carbachol, sodium azide, tetrahydrocannabinol, phenothiazines, and amphetamines into one or more sites. Three species of monkeys have been used: rhesus, green, and squirrel. The descriptive information available on each of these dyskinetic syndromes indicates a striking degree of similarity among the effects of these various drugs and combinations of drugs. The behavior patterns produced can be roughly divided into three areas: (1) increased movement (hyperkinesia) and vigilance, determined at least in part by the area in which the animal is confined; (2) a wide range of adventitious movements of extremities, as well as face and tongue; and (3) "stereotypic" behavior, sometimes destructive, such as grooming, biting, and drinking. None of the above studies or models has been employed in monkeys free-ranging in open areas with other animals. It might be expected that the effects of the drugs would be somewhat already by the social setting of the animal. It now seems adequately confirmed that the production of dyskinesia in monkeys is biochemically related to dopaminergic systems in the neostriatum. The evidence at present also points to a form of denervation hypersensitivity as the basis for the production of these syndromes in patients with dyskinesias on L-DOPA therapy (Chase, Holden, and Brody, 1972), although it is clear that in relatively high doses these drugs regularly produce dyskinesias in primates having no anatomical or biochemical pathology in the nervous system. These drug-induced dyskinesias in monkeys, especially those produced by L-DOPA in combination with other drugs or with anatomical and biochemical stereotaxically placed lesions, appear to be developed to a degree to be useful in the further evaluation of the mechanisms of dyskinesias in humans as well as providing methods of testing the effectiveness of various forms of therapy.