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Effects of lesions of the nucleus of the optic tract on optokinetic nystagmus and after-nystagmus in the monkey
Authors:D. Schiff  B. Cohen  J. Büttner-Ennever  V. Matsuo
Affiliation:(1) Departments of Neurology and Physiology and Biophysics, Mount Sinai School of Medicine, City University of New York, 1 East 100th Street, 10029 New York, NY, USA;(2) Mount Sinai School of Medicine, 1 East 100th Street, Annenberg 21-74, Box 1135, 10029 New York, NY, USA
Abstract: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.Abbreviations used in Figures 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
Keywords:Optokinetic nystagmus (OKN)  Optokinetic after-nystagmus (OKAN)  Velocity storage  Nucleus of the optic tract (NOT)  Dorsal terminal nucleus (DTN)  Monkey
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