The nucleus of the optic tract (NOT) is a visuopreoculomotor relay point responsible for optokinetic nystagmus (OKN).
1) In the present experiment, the effect of NOT lesions on both the rapid and the slow rise of OKN and optokinetic after-nystagmus (OKAN) was examined in 6 fuscata monkeys. In 3 monkeys with total NOT lesions no slow rise OKN velocity or OKAN was produced towards the side of the lesion. In one of the remaining 3 monkeys with partial NOT lesions, a slow rise in OKN and OKAN slow phase velocity were selectively reduced towards the side of the lesion. In all monkeys except for one which had marked spontaneus 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 influenced separately by NOT lesions : OKN and OKAN are abolished, but vestibular nystagmus remains unaffected.
2) To investigate how OKN signals descend and converge on the vestibular nucleus, biocytin was used as an anterograde tracer.
The pretectofugal fibers comprised of the following three pathways :
1 The NOT-contralateral NOT.
2 The NOT-the nucleus reticularis tegmenti pontis.
3 The NOT-the inferior olive, dorsal cap. The labeled fibers descended along the medial lemniscus to the medulla with axons branching out to the dorsolateral pontine nucleus, lateral part of the nucleus reticularis tegmenti pontis, nucleus prepositus hypoglossi, medial vestibular nucleus and finally the dorsal cap of the inferior olive ipsilateral to the injection site. The NOT efferent fibers terminated in the medial vestibular nucleus which could serve to drive the storage mechanisms.
