Nine monkeys were used in order to clarify the role of the nucleus of the optic tract (NOT) in the generation of optokinetic nystagmus (OKN). In 3 monkeys whose NOTs were almost totally damaged, optokinetic stimulus toward the lesioned side failed to generate either eye deviation or OKN and revealed only voluntary saccades, whereas that toward the side contralateral to the lesion generated normal gain of OKN. The phenomenon was identical in either monocular or binocular stimulation. In two of 3 monkeys whose NOTs were partially destroyed, optokinetic stimulus toward the lesioned side produced OKN, but the gain of OKN, but the gain of OKN was at maximum less than 60% in both binocular and monocular stimulation. In the remaining one monkey whose NOT was injured, but superficially, OKN showed normal gain in both directions. In 3 other monkeys whose NOTs were spared, this OKN asymmetry was not observed. Pursuit and saccadic eye movements were normal in all NOT-lesioned monkeys. Visually induced eye movements in the vertical axis were likewise normal. The present experiment suggests that the NOT in monkeys may be the first relay station in the horizontal optokinetic path and that in primates as in non-primates both crossed and uncrossed fibers reach motor centers for OKN via the NOT.