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Effects of lesions of the nucleus of the optic tract on optokinetic nystagmus and after-nystagmus in the monkey

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Summary

1. The nucleus of the optic tract (NOT) and the dorsal terminal nucleus (DTN) of the accessory optic system were lesioned electrolytically or with kainic acid in rhesus monkeys. When lesions involved NOT and DTN, peak velocities of optokinetic nystagmus (OKN) with slow phases toward the side of the lesion were reduced, and optokinetic after-nystagmus (OKAN) was reduced or abolished. The jump in slow phase eye velocity at the onset of OKN was smaller in most animals, but was not lost. Initially, there was spontaneous nystagmus with contralateral slow phases. OKN and OKAN with contralateral slow phases were unaffected. 2. Damage to adjacent regions had no effect on OKN or OKAN with two exceptions: 1. A vascular lesion in the MRF, medial to NOT and adjacent to the central gray matter, caused a transient loss of the initial jump in OKN. The slow rise in slow phase velocity was prolonged, but the gain of OKAN was unaffected. There was no effect after a kainic acid lesion in this region in another animal. 2. Lesions of the fiber tract in the pulvinar that inputs to the brachium of the superior colliculus caused a transient reduction in the buildup and peak velocity of OKN and OKAN. 3. In terms of a previous model (Cohen et al. 1977; Waespe et al. 1983), the findings suggest that the indirect pathway that activates the velocity storage integrator in the vestibular system to produce the slow rise in ipsilateral OKN and OKAN, lies in NOT and DTN. Activity for the rapid rise in OKN, carried in the direct pathway, is probably transmitted to the pontine nuclei and flocculus via an anatomically separate fiber path-way that lies in the MRF. A fiber tract in the pulvinar that inputs to the brachium of the superior colliculus appears to carry activity related to retinal slip from the visual cortex to NOT and DTN.

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Abbreviations

BIC:

brachium of the inferior colliculus

BSC:

brachium of the superior colliculus

C:

caudate nucleus

CG:

central gray

CL:

Centralis lateralis

dbc:

decussation of the brachium conjunctivum

DTN:

dorsal terminal nucleus of the accessory optic system

IC:

inferior colliculus

Hb:

habenular nucleus

hc:

habenular commissure

LD:

lateralis dorsalis

LGn:

lateral geniculate nucleus

MD:

medialis dorsalis

MGn:

medial geniculate nucleus

MLF:

median longitudinal fasciculus

MRF:

mesencephalic reticular formation

cMRF:

central mesencephalic reticular formation

NL:

nucleus limitans

NLL:

nucleus of the lateral lemniscus

NOT:

nucleus of the optic tract

PB:

parabigeminal nucleus

pc:

posterior commissure

Pi:

pineal gland

PON:

pretectal olivary nucleus

Pt:

pretectum

Pulv:

pulvinar

R:

nucleus reticularis

RN:

red nucleus

RpN:

raphe nucleus

RTP:

nucleus reticularis tegmenti pontis

SC:

superior colliculus

SCpit:

superior cerebellar peduncle

VPL:

ventralis postero-lateralis

VPM:

ventralis posteromedialis

III:

oculomotor nucleus

IV:

trochlear nucleus

IVn:

trochlear nerve

Vm:

mesencephalic trigeminal nucleus

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Schiff, D., Cohen, B., Büttner-Ennever, J. et al. Effects of lesions of the nucleus of the optic tract on optokinetic nystagmus and after-nystagmus in the monkey. Exp Brain Res 79, 225–239 (1990). https://doi.org/10.1007/BF00608231

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  • DOI: https://doi.org/10.1007/BF00608231

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