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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basic properties of responses to visual stimulation with large moving random dot patterns were studied in ferret nucleus of the optic tract. Retinal input to NOT was assessed by orthodromic electrical stimulation of the optic chiasm and optic nerves. Presence of an input from visual cortex was tested by orthodromic electrical stimulation of ipsilateral area 17. All 51 NOT neurons studied displayed a non-habituating, clearly direction-specific response: discharge rate strongly increased with the stimulus pattern moving horizontally in ipsiversive direction (motion directed towards the recorded hemisphere) and decreased with contraversive stimulus motion. Most latencies to visual stimulation ranged from 80 to 100 ms. Velocity tuning was studied using stimulus velocities between 4 deg/s and 100 deg/s. Discharge rates were most effectively modulated at a stimulus velocity of 20 deg/s. A large portion of the cells studied (91%) could be binocularly activated, although for almost all neurons the contralateral eye was dominant. Through stimulation of the optic chiasm 46 out of 51 NOT neurons could be electrically activated with a latency of 5.42 +/- 0.66 ms (mean +/- SD). For 15 fibers stimulated from both optic chiasm and contralateral optic nerve, conduction velocities between 2.5 and 8.9 m/s, with a mean of 5.1 m/s, were obtained. A major direct input from the ipsilateral retina was not found. Furthermore, 65% of all neurons could be activated through electrical stimulation of visual cortex with a mean latency of 3.7 +/- 1.5 ms, indicating a strong cortical projection to ferret NOT. The functional relevance of response properties of ferret NOT neurons for horizontal optokinetic nystagmus is discussed. Parameters that could be related to formation of a cortico-pretectal projection in mammals are considered.
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PMID:Visual response properties and afferents of nucleus of the optic tract in the ferret. 207 37

1. The role of the pretectal NOT and the DTN in producing horizontal OKN and OKAN were studied using electrical stimulation and lesions. Positive stimulation sites lay in NOT, DTN, and in a fiber bundle in the pulvinar that is presumably a cortical input to NOT. 2. When the region of NOT was electrically stimulated in darkness, horizontal nystagmus was evoked with ipsilateral slow phases. Eye velocity rose slowly to a steady-state level and was followed by afternystagmus at the end of stimulation. The time constant of rise of stimulus-induced nystagmus was similar to the slow rise of slow-phase eye velocity during OKN. The saturation velocity of the induced nystagmus and the falling time constant of the stimulus afternystagmus were the same as those of OKAN. This suggests that electrical stimulation of NOT and DTN had elicited the slow component of OKN, i.e., that component produced by the velocity storage mechanism in the vestibular system. 3. Consistent with this postulate, activity induced by NOT stimulation could enhance, prolong, or block the slow component of OKN and OKAN depending on whether slow phases were to the same or opposite side. Stimulus-induced activity also interacted with vestibular nystagmus as would OKN and OKAN. 4. Unilateral lesions of NOT and DTN caused a loss of OKAN and the slow rise in OKN to the ipsilateral side. Steady-state velocities of OKN were reduced. The initial jump of OKN slow-phase velocity was the same or somewhat less after lesions but was not lost. 5. Partial lesions of a fiber bundle in the lateral pulvinar caused a transient change in OKN and OKAN, consistent with the idea that it carries activity for the slow component from the cortex to NOT. A lesion of the MRF, just rostral to the superior colliculus, caused a transient loss of the rapid component of OKN. This region appears to carry activity responsible for the initial jump in slow-phase velocity at the onset of stimulation. 6. We conclude that: (a) NOT and probably DTN lie in the indirect pathway that produces the slow component of horizontal OKN and OKAN to the ipsilateral side in the rhesus monkey. This pathway activates the velocity storage mechanism in the vestibular nuclei. (b) At the level of NOT, the pathway responsible for the slow component of OKN and OKAN is anatomically distinct from the pathway responsible for rapid changes in eye velocity at the onset of OKN.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Contribution of the nucleus of the optic tract to optokinetic nystagmus and optokinetic afternystagmus in the monkey: clinical implications. 210 53

Large numbers of neurons were retrogradely labeled in both the dorsal and ventral medial terminal nucleus (MTN) after fluoro-gold injections into the rat pretectal nucleus of the optic tract/dorsal terminal nucleus (NOT/DTN). Fluorescence immunocytochemistry for GABA in the same brains revealed GABA-positive neurons distributed mainly in the dorsal MTN. Approximately half of all the GABAergic neurons in the MTN were double-labeled. Therefore, GABAergic neurons comprise a significant component of the MTN-NOT/DTN projection which most likely inhibits the pretectal pathway mediating horizontal optokinetic nystagmus.
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PMID:The projection of GABA-ergic neurons of the medial terminal accessory optic nucleus to the pretectum in the rat. 213 69

It has been previously assumed that the asymmetry of the monocular optokinetic nystagmus (OKN) of lateral-eyed mammals is caused by an absence of visual cortex projections to directional selective neurons in the pretectal nucleus of the optic tract and dorsal terminal nucleus of the accessory optic system (NOT-DTN). In contrast to this generally accepted hypothesis, we present multiple evidence that OKN-related neurons in the rat NOT-DTN in fact do receive input from the visual cortex. We studied the corticofugal projection to NOT-DTN physiologically, with extracellular single unit recording and electrical stimulation of the optic chiasma and the visual cortex, and anatomically, using retrograde and anterograde tracing techniques. In particular we focussed our attention on the NOT-DTN neurons, which control eye movements during OKN. All OKN-related NOT-DTN cells were activated after optic chiasma stimulation. Forty-five percent of these neurons were also activated after stimulation of the visual cortex (VC). The majority of neurons activated from VC (80%) also responded to monocular stimulation of either eye. On the contrary, most of the neurons that responded to stimulation of the contralateral eye only were not activated from VC. After injection of fluorescent latex microspheres into the NOT-DTN, retrogradely labeled neurons were found in areas 17, 18, and 18A of the visual cortex. Phaseolus vulgaris leucoagglutinin injected into the visual cortex anterogradely labeled fibres and terminals throughout the NOT-DTN complex. Labeled boutons were found in close proximity to OKN-related NOT-DTN cells, selectively stained after horseradish peroxidase (HRP) injections into the inferior olive. Our results demonstrate that NOT-DTN cells in the rat, which are involved in the generation of horizontal OKN, receive a direct input from the ipsilateral visual cortex.
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PMID:OKN-related neurons in the rat nucleus of the optic tract and dorsal terminal nucleus of the accessory optic system receive a direct cortical input. 849 67

Horizontal optokinetic nystagmus (OKN) as well as neuronal response properties in the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system (NOT-DTN) were investigated in three monocularly deprived squirrel monkeys. In two monkeys occlusion of one eye was performed at birth (early) and in the third after 7 weeks (late). In adulthood, in early deprived monkeys monocular horizontal OKN tested through the non-deprived eye was symmetrical and in no way different from normal, i.e. stimulation in the temporonasal and nasotemporal direction elicited equal and robust responses. OKN through the early occluded eye, however, was grossly abnormal with low gain and great variability in the consistency of nasotemporal and temporonasal slow phase eye movements. When in the late deprived monkey the non-deprived eye was occluded a strong spontaneous nystagmus developed despite the deprived eye viewing a stationary pattern. The slow phases were directed from nasal to temporal for the deprived eye. When tested through the non-deprived eye all neuronal responses of the NOT-DTN were normal. The deprived eye's influence on NOT-DTN neurons was extremely weak. No neuron with a moderate or even dominant input from the deprived eye was found after early deprivation. In the late deprived case the deficit was not as severe but still the non-deprived eye was clearly dominating the responses in all neurons tested. Velocity tuning of neurons tested through the non-deprived eye was normal and qualitatively corresponded well to slow phase eye velocity in response to equivalent retinal slip during OKN. Through the early deprived eye, however, velocity tuning was extremely poor. It was somewhat better through the late deprived eye. We suggest that the dramatic deterioration in the optokinetic reflex found after long-term monocular deprivation for the amblyopic eye is probably caused by the almost complete loss of retinal and cortical input driven by that eye to the NOT-DTN. These results are discussed in relation to our previous results in cats and reports in the literature for humans with occlusion amblyopia.
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PMID:Optokinetic reflex in squirrel monkeys after long-term monocular deprivation. 975 82

Eye position and angular velocity were measured in squirrel monkeys (Saimiri sciureus) by means of the electromagnetic scleral search-coil technique. Horizontal sigma-optokinetic nystagmus (sigma-OKN) was elicited by a stationary, stroboscopically illuminated, periodic, vertical-stripe pattern lining a vertical cylinder. The relationship between the mean slow-phase eye angular velocity, Ve, of sigma-OKN and the product of pattern period, Ps, and flash frequency, f(s), was determined. When Ve approximated k x Ps x f(s) (deg x s(-1)) and k was an integer > or = 1, the sigma-paradigm was fulfilled. Sigma-OKN could be evoked in different "modes", whereby k approximated 1, 2,...n. The sigma-OKN properties of squirrel monkeys were similar to those measured for sigma-OKN in the "stare" mode in man, with the exception of a long-lasting optokinetic afternystagmus (sigma-OKAN) appearing in the monkey. A considerable amount of temporal variability in flash sequence intervals ("temporal noise"), causing retinal error signals that interfered with the sigma-paradigm, was accepted by the visuo-motor system without interruption of sigma-OKN. This observation was explained by the operation of a short memory device for perception of visual motion. The internal gain, g(i), which relates the retinal "error" displacement velocity, Vr, and Ve depended, in turn, on Vr according to a function resembling the known relationship between neuronal activity of NOT (nucleus of the optic tract) nerve cells and Vr. This observation may be taken as direct proof that sigma-OKN can be explained by a centrally preprogrammed relationship between the retinal velocity, Vr, and the OKN slow-phase eye velocity, Ve. It is stipulated that the sum of Vr and efference copy signals generated in cortical or subcortical gaze centers is the essential component controlling the perceived velocity of the sigma-movement, whereby a short-term integrator plays a role for squirrel monkey sigma-OKN. When the flash frequency, f(s), was modulated periodically according to a sinewave or "triangular" function at a rate below 0.5 cycles x s(-1), Ve was found to respond with a corresponding modulation, provided the modulation amplitude did not exceed 50% of the mean flash rate. When the latter occurred, nonlinear responses could be observed. A similar response was found when the speed of "real" optokinetic stimuli was varied sinusoidally. Under these experimental conditions, however, the amplitude of the Ve variation yielded up to 1.0 approximately linear responses.
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PMID:Sigma-optokinetic nystagmus in squirrel monkeys elicited by stationary stripe patterns illuminated by regular and random-interval flash sequences. 1009 Jun 57

Using classical neuroanatomical retrograde tracing methods we investigated the retinal ganglion cells projecting to the nucleus of the optic tract and dorsal terminal nucleus of the accessory optic system (NOT-DTN) in macaque monkeys. Our main aim was to quantify the strength of the projection from the ipsilateral retina to the NOT-DTN. We therefore examined the number, distribution, and soma size of retinal ganglion cells involved in this projection. Electrophysiologically controlled small injections into the NOT-DTN revealed a clearly bilateral retinal projection originating mainly from the central retina but also involving peripheral retinal regions. Labelled cells were found nasally in the contralateral retina and temporally in the ipsilateral retina with some overlap in the fovea. The projection from the ipsilateral retina was 36-43% of that from the contralateral retina. On average, only 1-6% of the local population of ganglion cells projected to the NOT-DTN. Small soma size and large dendritic fields imply that in monkey rarely encountered, 'specialized' ganglion cells provide the direct retinal input to the accessory optic system (AOS). These results are discussed with respect to the symmetry of monocular horizontal optokinetic nystagmus (OKN) in primates.
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PMID:Retinal ganglion cells projecting to the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system in macaque monkeys. 1094 15

The goal of the present investigation was to elucidate the role of the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system (NOT-DTN) for slow eye movements other than horizontal. Retinal slip neurons in the NOT-DTN in the awake behaving cat respond direction selectively to the ipsiversive component of horizontal and oblique image motion. They are, however, influenced neither by pure vertical stimulus movement nor by eye movements in the dark. Electrical stimulation of the NOT-DTN leads to pure horizontal optokinetic nystagmus with ipsiversive slow phases and does not influence vertical eye position. In addition, unilateral reversible inactivation of the NOT-DTN with muscimol elicits spontaneous contraversive horizontal nystagmus without vertical component. During oblique optokinetic stimulation, the ipsiversive OKN component is significantly decreased in all directions. After bilateral NOT-DTN inactivation, OKN can only be elicited in a narrow range of upward directions. These data indicate that the NOT-DTN is the only source to drive the horizontal component of OKN.
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PMID:Directional effect of inactivation of the nucleus of the optic tract on optokinetic nystagmus in the cat. 1171 81

We compared the horizontal optokinetic reaction (OKR) and response properties of retinal slip neurons in the nucleus of the optic tract and dorsal terminal nucleus (NOT-DTN) of albino and wild-type ferrets (Mustela putorius furo). In contrast to pigmented ferrets, we were unable to observe OKR in albino ferrets during binocular and monocular viewing using random dot full field stimulation and electro-oculography (EOG). Observations during early postnatal life indicate that regular OKR is present in pigmented pups 3 d after eye opening but is absent at any stage during development in albino ferrets. Unilateral muscimol injections to inactivate all neurons in the NOT-DTN containing GABA(A) and GABA(C) receptors caused spontaneous horizontal nystagmus with slow phases away from the injected hemisphere in albino as well as in pigmented animals. Retinal slip neurons in the NOT-DTN of albino ferrets identified by antidromic activation from the inferior olive and orthodromic activation from the optic chiasm were well responding to intermittent bright light stimuli, but many showed a profound reduction of responsiveness to moving stimuli. The movement-sensitive neurons exhibited no clear direction selectivity for ipsiversive stimulus movement, a characteristic property of these neurons in pigmented ferrets and other mammals. Thus, the defect rendering albino ferrets optokinetically nonresponsive is located in the visual pathway subserving the OKR, namely in or before the NOT-DTN, and not in oculomotor centers.
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PMID:Optokinetic deficits in albino ferrets (Mustela putorius furo): a behavioral and electrophysiological study. 1510 21

The optokinetic reflex and neuronal response properties in the central visual pathway were studied in three macaque monkeys (Macaca nemestrina) with early childhood strabismus of various origin. Binocularity in the primary visual cortex (VI) measured electrophysiologically was reduced both in a monkey with resolved strabismus and in a monkey with accommodative strabismus when compared to normal controls. By contrast, binocularity in the nucleus of the optic tract and dorsal terminal nucleus of the accessory optic system (NOT-DTN) was only reduced in the monkey with resolved strabismus ('resolved'), but appeared normal in animals with accommodative strabismus ('accom. 1 'and 'accom. 2'). Sub-threshold binocular interactions were normal in all animals. The velocity tuning curves of retinal slip neurons in the NOT-DTN of all strabismic monkeys were not different from normal controls. Horizontal optokinetic nystagmus was asymmetric in monkey 'accom. 2', and for the non-fixating eye in monkey 'resolved'. In monkey 'accom. 1' OKN was normal. Open loop eye velocity was lower in the monkey with resolved strabismus than in monkeys with accommodative strabismus. These data suggest that different causes of strabismus may affect neuronal response properties and behavior to different degrees. The effects on the optokinetic reflex of resolved, but early onset strabismus were more severe than those of accommodative strabismus. This corresponds to the wide variability of defects in the optokinetic system of strabismic humans.
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PMID:Neuronal basis of optokinetic reflex pathology in naturally strabismic monkeys. 2131 6


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