A previous experiment disclosed that unilateral lesions of the nucleus of the optic tract (NOT) in the fascicularis monkey resulted in selective loss of optokinetic nystagmus (OKN) towards the lesioned side. This may suggest that the NOT in monkeys, as in non-primates, represents the first relay station in the basic horizontal optokinetic path. This monkey, however, did not show a rapid rise in OKN velocity in response to steps in stimulus velocity. In the present experiments, effects of NOT lesions upon both the rapid and the slow rise of OKN as well as optokinetic after-nystagmus (OKAN) were examined in 6 fuscata monkeys. In 3 with total NOT lesions of 6 monkeys, none of the slow rise OKN or OKAN slow phase velocity were produced towards the lesioned side. In one of the remaining 3 monkeys with partial NOT lesions, a slow rise OKN and OKAN slow phase velocity were selectively reduced towards the lesioned side. In 2 of these 4 monkeys whose lesions were localized in the lateral portions of the pretectum, rapid rise in OKN velocity remained unchanged, whereas in the remaining two whose lesions were large enough to extend into the medial portions of the pretectum near the nucleus of the posterior commissure, rapid rise in OKN velocity was reduced. In the remaining 2 monkeys whose NOT was only superficially damaged, all components of OKN were normal. Other visually induced eye movements were normal. In all monkeys except for one who had marked spontaneous nystagmus, the peak velocity of vestibular nystagmus was not affected after NOT lesions. These findings indicate that the dynamics of the charge of the velocity storage mechanism is separately influenced by NOT lesions: OKN and OKAN are abolished, but vestibular nystagmus remains unaffected.