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The nucleus of the optic tract. Its function in gaze stabilization and control of visual-vestibular interaction1. Electrical stimulation of the nucleus of the optic tract (NOT) induced nystagmus and after-nystagmus with ipsilateral slow phases. The velocity characteristics of the nystagmus were similar to those of the slow component of optokinetic nystagmus (OKN) and to optokinetic after-nystagmus (OKAN), both of which are produced by velocity storage in the vestibular system. When NOT was destroyed, these components disappeared. This indicates that velocity storage is activated from the visual system through NOT. 2. Velocity storage produces compensatory eye-in-head and head-on-body movements through the vestibular system. The association of NOT with velocity storage implies that NOT helps stabilize gaze in space during both passive motion and active locomotion in light with an angular component. It has been suggested that "vestibular-only" neurons in the vestibular nuclei play an important role in generation of velocity storage. Similarities between the rise and fall times of eye velocity during OKN and OKAN to firing rates of vestibular-only neurons suggest that these cells may receive their visual input through NOT. 3. One NOT was injected with muscimol, a GABAA agonist. Ipsilateral OKN and OKAN were lost, suggesting that GABA, which is an inhibitory transmitter in NOT, acts on projection pathways to the brain stem. A striking finding was that visual suppression and habituation of contralateral slow phases of vestibular nystagmus were also abolished after muscimol injection. The latter implies that NOT plays an important role in producing visual suppression of the VOR and habituating its time constant. 4. Habituation is lost after nodulus and uvula lesions and visual suppression after lesions of the flocculus and paraflocculus. We postulate that the disappearance of vestibular habituation and of visual suppression of vestibular responses after muscimol injections was due to dysfacilitation of the prominent NOT-inferior olive pathway, inactivating climbing fibers from the dorsal cap to nodulouvular and flocculoparafloccular Purkinje cells. The prompt loss of habituation when NOT was inactivated, and its return when the GABAergic inhibition dissipated, suggests that although VOR habituation can be relatively permanent, it must be maintained continuously by activity of the vestibulocerebellum.
Document ID
20050000695
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Cohen, B.
(Mount Sinai School of Medicine New York, New York 10029)
Reisine, H.
Yokota, J. I.
Raphan, T.
Date Acquired
August 22, 2013
Publication Date
May 22, 1992
Publication Information
Publication: Annals of the New York Academy of Sciences
Volume: 656
ISSN: 0077-8923
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: EY01867
CONTRACT_GRANT: EY04148
CONTRACT_GRANT: EY02296
Distribution Limits
Public
Copyright
Other
Keywords
Review
Non-NASA Center
NASA Discipline Neuroscience
Review, Tutorial

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