The effects of lesions of the nucleus of optic tract on the optokinetic nystagmus in monkeys

Abstract

The nucleus of optic tract (NOT) is considered as an essential premotor area for the generation of optokinetic nystagmus (OKN) in afoveate animals. In the primates, however, very little information on the optokinetic (OK) subcortical pathway, either anatomically or physiologically, is available. In order to clarify the role of the NOT in generation of OKN, the lateral pretectum including the NOT were destroyed by surgical knife or electrolytic device in nine monkeys (Macaca Fascicularis). In three monkeys whose NOTs were totally damaged, OKN were totally abolished against optokinetic (OK) stimulation toward the side of lesion, whereas OK stimulation toward the contralateral side generated the normal gain of OKN. This phenomenon was identical in both monocular and binocular stimulation. In two monkeys with partial NOT-lesions, OKN were produced against OK stimulation toward the side of lesion, but gain of OKN was less than 0.6. In four other monkeys whose NOTs were spared, OK stimulation in both directions generated the normal gain of OKN. Smooth pursuit and saccade were normal in all NOT-lesioned monkeys.Consequently, the present study suggests that the NOT in monkey will be the first relay station in the OKN same as in non-primates, and the functional pathways of OKN and other visually induced eye movements may be separate at the level of the NOT.