Effects of accessory optic system lesions on vestibulo-ocular and optokinetic reflexes in the cat

Summary Horizontal vestibulo-ocular reflex (VOR) and optokinetic nystagmus (OKN) were studied before and after lesions within the accessory optic system (AOS) in the cat. Post-lesion retinal input to the AOS was evaluated using the autoradiographic technique. Unilateral lesion of the lateral terminal nucleus of the AOS (LTN) and the resulting retinal deafferentation of the medial terminal nucleus of the AOS (MTN) induced a spontaneous nystagmus in the dark whose slow phase was directed ipsilaterally to the lesion. VOR gain was reduced for both directions with a maximal decrease for stimulation directed ipsilaterally to the lesion. OKN gain obtained for both directions of binocular stimulation was decreased, mainly when the stimulus was directed contralaterally to the lesion. After two postoperative weeks, spontaneous nystagmus disappeared and the VOR symmetry recovered simultaneously. A symmetrical OKN was only observed after one month. In spite of the known visual selectivity for vertical direction in LTN-MTN cells, the results of this study support a functional involvement of these nuclei in horizontal VOR and OKN.Supported by C.N.R.S. (ATP N 8115)     

Modification of the balance and gain of the vestibulo-ocular reflex in the cat

Summary The characteristics of the vestibulo-ocular reflex (VOR) of a normal cat can be modified in response to visual demands. Two aspects of the VOR are modifiable independently by a normal cat: the gain and the balance. An imbalance results in a spontaneous nystagmus and an asymmetric VOR. Neither the gain nor the balance of a dark-reared cat's VOR is susceptible to visual modification. A cat whose crossed visual pathways are severed at the level of the optic chiasm is able to modify the gain of the VOR but not its balance. Both dark-reared and split-chiasm cats have only very short-lasting optokinetic after-nystagmus.This research was supported by USPHS grant EY02248 and grants from the M.R.C. (MT5201) and NSERC (A9949) of CanadaDr. L. R. Harris was in receipt of a Wellcome travel grant     

Slow eye movements induced by apparent target motion in monkey

Summary Slow eye movements were observed while the monkey fixated on a subject-stationary, small target light in front of a moving optokinetic drum in an attempt to suppress optokinetic nystagmus (OKN). These slow eye movements of low amplitude were directed opposite to the moving optokinetic stimulus and, hence, were not identical to slow phases of incompletely suppressed OKN. It is assumed, based on comparable findings in humans, that these slow eye movements are induced by a perceived target motion, i.e. by the perception of an apparent motion of the subject-stationary fixation light opposite to the actual motion of the optokinetic drum.Supported by a grant from the Swiss National Foundation (3.510-0.86)     

Contribution of eye muscle proprioception to velocity-response characteristics of eye movements: involvement of the cerebellar flocculus.

The vestibulo-ocular reflex (VOR) and optokinetic nystagmus (OKN) were examined in alert pigmented rabbits following interruption of proprioceptive afferents from the extraocular muscles in one eye by surgical section of the ophthalmic branch of the trigeminal nerve (V1 nerve). Deficits were mainly produced in movement dynamics of the ipsilateral eye including reduction of (1) the VOR gain at a high frequency of head rotation, (2) the OKN gain and (3) the velocity of quick eye movements in the OKN. In some of the rabbits examined, the cerebellar flocculus was lesioned by local injection of kainic acid before severance of the V1 nerve. No significant additional reductions of VOR or OKN gains were produced by V1 nerve section in the flocculus-lesioned rabbits. These results suggest that proprioceptive signals from eye muscles act to improve VOR and OKN dynamics through the neuronal mechanisms involving the cerebellar flocculus.     

Spontaneous nystagmus and gaze-holding ability in monkeys after intravitreal picrotoxin injections.

1. Eye movements were measured in three rhesus monkeys after monocular intravitreal injections of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist. The effects of this drug were tested when the animals were in a completely dark room, when they performed a smooth pursuit task, and when they viewed either a stationary pattern or a full-field optokinetic pattern rotating horizontally. 2. Between 15 and 20 min after the injection, a sustained conjugate spontaneous nystagmus developed in the dark, with the slow-phase movement in the temporal-to-nasal direction with respect to the injected eye. Peak slow-phase velocity ranged from 15 to 45 degrees/s. The nystagmus persisted for at least 1 h but stopped by the next day. 3. In a well-lit room, the nystagmus was completely suppressed, even during monocular viewing with the injected eye. When the lights were turned off, the slow-phase velocity of the spontaneous nystagmus slowly increased to a steady-state level within 70-120 s. 4. Horizontal smooth pursuit eye movements to a 1 degree target light moving in front of the animal +/- 20 degrees to either side of center of gaze at constant speeds were normal. Target speeds ranging from 15 to 60 degrees/s for both monocular and binocular viewing conditions were used. Binocular and monocular optokinetic nystagmus (OKN) to a full-field drum rotating at a constant velocity (5-90 degrees/s) were also normal. The initial pursuit and steady-state components of OKN were measured, as well as the velocity-storage component (optokinetic after nystagmus, OKAN).(ABSTRACT TRUNCATED AT 250 WORDS)     

Gaze-stabilizing deficits and latent nystagmus in monkeys with brief, early-onset visual deprivation: eye movement recordings

The normal development and the capacity to calibrate gaze-stabilizing systems may depend on normal vision during infancy. At the end of 1 yr of dark rearing, cats have gaze-stabilizing deficits similar to that of the newborn human infant including decreased monocular optokinetic nystagmus (OKN) in the nasal to temporal (N-T) direction and decreased velocity storage in the vestibuloocular reflex (VOR). The purpose of this study is to determine to what extent restricted vision during the first 2 mo of life in monkeys affects the development of gaze-stabilizing systems. The eyelids of both eyes were sutured closed in three rhesus monkeys (Macaca mulatta) at birth. Eyelids were opened at 25 days in one monkey and 40 and 55 days in the other two animals. Eye movements were recorded from each eye using scleral search coils. The VOR, OKN, and fixation were examined at 6 and 12 mo of age. We also examined ocular alignment, refraction, and visual acuity in these animals. At 1 yr of age, visual acuity ranged from 0.3 to 0.6 LogMAR (20/40-20/80). All animals showed a defect in monocular OKN in the N-T direction. The velocity-storage component of OKN (i.e., OKAN) was the most impaired. All animals had a mild reduction in VOR gain but had a normal time constant. The animals deprived for 40 and 55 days had a persistent strabismus. All animals showed a nystagmus similar to latent nystagmus (LN) in human subjects. The amount of LN and OKN defect correlated positively with the duration of deprivation. In addition, the animal deprived for 55 days demonstrated a pattern of nystagmus similar to congenital nystagmus in human subjects. We found that restricted visual input during the first 2 mo of life impairs certain gaze-stabilizing systems and causes LN in primates.     

Unidirectional habituation of vestibulo-ocular responses by repeated rotational or optokinetic stimulations in the cat

Summary 1.Unilateral habituation of the vestibuloocular reflex was produced in adult cats stimulated by repeated unidirectional velocity steps (vestibular training) or by a continuously moving visual surround (optokinetic training). — 2. Unidirectional vestibular training produced a strong asymmetry of vestibuloocular responses (VOR). Responses to velocity steps applied to the trained labyrinth were decreased both in gain and in time-constant. This effect generalized to responses to sinusoidal oscillations (0.03 Hz to 0.1 Hz), i.e. to a stimulus not used during training. — No spontaneous nystagmus was ever observed in spite of the dynamic VOR asymmetry. — 3. Unilateral vestibular habituation produced by vestibular training appeared to be a long-lasting phenomenon. It was still present 10 days after the end of training. — 4. Optokinetic responses were not affected by vestibular training. — 5. Unidirectional optokinetic training produced an increase in the slow phase velocity of optokinetic nystagmus (OKN) by about 25% in both directions. This effect did not persist for more than a few minutes. A marked spontaneous nystagmus was recorded in the dark after each session of optokinetic training, with a slow phase in the direction opposite to the previous OKN. — 6. VOR in response to velocity steps and to sinusoidal oscillations were decreased unilaterally after optokinetic training. This effect was of short duration, however, and disappeared within the interval between training sessions. This lack of retention contrasted with the prolonged effect of vestibular training.Supported by INSERM (France) and by CNR (Italy)     

Afternystagmus in darkness after suppression of optokinetic nystagmus: an interaction of motion aftereffect and retinal afterimages

The afternystagmus that occurs in the dark after gaze fixation during optokinetic stimulation is directed in the opposite direction relative to the previous optokinetic stimulus. The mechanism responsible for such afternystagmus after suppression of optokinetic nystagmus (ASOKN) is unclear. Several hypotheses have been put forward to explain it, but none is conclusive. We hypothesized that ASOKN is driven by the interaction of two mechanisms: (1) motion-aftereffect (MAE)-induced eye movements and (2) retinal afterimages (RAIs) produced by fixation during the suppression of optokinetic nystagmus (OKN). We examined the correlation among ASOKN, MAE-induced eye movements, and RAIs in healthy subjects. Adapting stimuli consisted of moving random dot patterns and a fixation spot and their brightness was adjusted to induce different RAI durations. Test patterns were a stationary random dot pattern (to test for the presence of a MAE), a dim homogeneous background (to test for MAE driven eye movements), and a black background (to test for ASOKN and RAIs). MAEs were reported by 16 out of 17 subjects, but only 7 out of 17 subjects demonstrated MAE-induced eye movements. Importantly, ASOKN was only found when these seven subjects reported a RAI after suppression of OKN. Moreover, the duration of ASOKN was longer for high-brightness stimuli compared with low-brightness stimuli, just as RAIs persist longer with increasing brightness. We conclude that ASOKN results from the interaction of MAE-induced eye movements and RAIs.     

Influence of otolithic stimulation by horizontal linear acceleration on optokinetic nystagmus and visual motion perception

Summary Several studies in the past have demonstrated the existence of an Otolith-Ocular Reflex (OOR) in man, although much less sensitive than canal ocular reflex. The present paper 1 confirms these previous results. Nystagmic eye movements (L-nystagmus) appear in the seated subject during horizontal acceleration along the interaural axis in the dark for an acceleration level (1 m/s²) about ten times the perception threshold with a sensitivity of about 0.035 rad/m.When sinusoidal linear acceleration is combined with optokinetic stimulation, the recorded nystagmus slow phase velocity exhibits strong periodic modulation related to subject motion. This marked effect of linear acceleration on the optokinetic nystagmus (OKN) appears at a level (0.1 m/s²) close to the acceleration perception threshold and has a 4-fold higher sensitivity than L-nystagmus. Modulation of OKN can reach a peak-to-peak amplitude as great as 20 °/s; for a given optokinetic field size it increases with the velocity of the optokinetic stimulus, i.e. with the slow phase eye velocity. In parallel with changes in OKN slow phase velocity, linear acceleration induces a motion related decrease in the perceived velocity of the visual scene and modifications in selfmotion perception.The results are interpreted in terms of a mathematical model of visual-vestibular interaction. They show that sensory interaction processes can magnify the contribution given to the control of eye movements by the otolithic system and provide a way of exploring its function at low levels of acceleration.The present work has been presented at III European Neurosciences Meeting, Rome, September 1979     

Optokinetic-vestibular interaction in patients with increased gain of the vestibulo-ocular reflex

We studied optokinetic nystagmus (OKN), optokinetic afternystagmus (OKAN) and visual-vestibular interaction in five patients with markedly elevated vestibulo-ocular reflex (VOR) gain due to cerebellar atrophy. All had impaired smooth pursuit, decreased initial slow phase velocity of OKN, and impaired ability to suppress the VOR with real or imagined targets. OKN slow phase velocity gradually built up over 25–45 s, reaching normal values for low stimulus velocities (30 deg/s). Initial velocity of OKAN was increased, but the rate of decay of OKAN was normal. These findings can be explained by models that include separate velocity storage and variable gain elements shared by the vestibular and optokinetic systems.     

Optokinetic nystagmus in the ferret: including selected comparisons with the cat

Summary The aim of this study was to evaluate the functional significance of similarities observed in the anatomy and the physiology of cat and ferret visual systems. Optokinetic nystagmus (OKN) in response to movement of the entire visual field, and optokinetic after nystagmus (OKAN) were measured in 8 ferrets with binocular stimulation. A shift of the beating field in the same direction as the fast phase of eye movements was observed both in ferret and cat. The absence of a fast rise in slow phase velocity (SPV) and similarities in the time constant to reach the steady state OKN gain, using step velocity stimuli are noted. As in the cat, primary OKAN was observed with a gradual decrease in its SPV. Following termination of stimulation, no sudden fall in SPV was noted for either species. However, for the ferret, the decrease was more rapid. With monocular stimulation, small differences were observed in OKN gain when responses to temporonasal and nasotemporal directions of the stimulus were compared in the two species. In contrast, the ferret displays a OKN gain which is approximatively twice that of the cat at stimulus velocities of 100°/sec. Even at 200°/sec., visual movement still induces a discernable OKN response (gain.0.07). Secondary OKAN, always present in the cat, was observed in only 43% of ferret records. Taken together with other considerations, these findings recommend the ferret as an alternative to the cat for the study of OKN and of other visuo-motor capacities in carnivores.     

Eye movement deficits following ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys II. Pursuit, vestibular, and optokinetic responses

The eyes are moved by a combination of neural commands that code eye velocity and eye position. The eye position signal is supposed to be derived from velocity-coded command signals by mathematical integration via a single oculomotor neural integrator. For horizontal eye movements, the neural integrator is thought to reside in the rostral nucleus prepositus hypoglossi (nph) and project directly to the abducens nuclei. In a previous study, permanent, serial ibotenic acid lesions of the nph in three rhesus macaques compromised the neural integrator for fixation but saccades were not affected. In the present study, to determine further whether the nph is the neural substrate for a single oculomotor neural integrator, the effects of those lesions on smooth pursuit, the vestibulo-ocular reflex (VOR), vestibular nystagmus (VN), and optokinetic nystagmus (OKN) are documented. The lesions were correlated with long-lasting deficits in eye movements, indicated most clearly by the animals' inability to maintain steady gaze in the dark. However, smooth pursuit and sinusoidal VOR in the dark, like the saccades in the previous study, were affected minimally. The gain of horizontal smooth pursuit (eye movement/target movement) decreased slightly (<25%) and phase lead increased slightly for all frequencies (0.3-1.0 Hz, +/-10 degrees target tracking), most noticeably for higher frequencies (0.8-0.7 and approximately 20 degrees for 1.0-Hz tracking). Vertical smooth pursuit was not affected significantly. Surprisingly, horizontal sinusoidal VOR gain and phase also were not affected significantly. Lesions had complex effects on both VN and OKN. The plateau of per- and postrotatory VN was shortened substantially ( approximately 50%), whereas the initial response and the time constant of decay decreased slightly. The initial OKN response also decreased slightly, and the charging phase was prolonged transiently then recovered to below normal levels like the VN time constant. Maximum steady-state, slow eye velocity of OKN decreased progressively by approximately 30% over the course of the lesions. These results support the previous conclusion that the oculomotor neural integrator is not a single neural entity and that the mathematical integrative function for different oculomotor subsystems is most likely distributed among a number of nuclei. They also show that the nph apparently is not involved in integrating smooth pursuit signals and that lesions of the nph can fractionate the VOR and nystagmic responses to adequate stimuli.     

The effects of head and trunk position on torsional vestibular and optokinetic eye movements in humans

We measured torsional vestibular and optokinetic eye movements in human subjects with the head and trunk erect, with the head supine and the trunk erect, and with the head and trunk supine, in order to quantify the effects of otolithic and proprioceptive modulation. During active head movements, the torsional vestibulo-ocular reflex (VOR) had significantly higher gain with the head upright than with the head supine, indicating that dynamic otolithic inputs can supplement the semicircular canal-ocular reflex. During passive earth-vertical axis rotation, torsional VOR gain was similar with the head and trunk supine and with the head supine and the trunk erect. This finding implies that static proprioceptive information from the neck and trunk has little effect upon the torsional VOR. VOR gain with the head supine was not increased by active, self-generated head movement compared with passive, whole body rotation, indicating that the torsional VOR is not augmented by dynamic proprioceptive inputs or by an efference copy of a command for head movement. Viewing earth-fixed surroundings enhanced the torsional VOR, while fixating a chair-fixed target suppressed the VOR, especially at low frequencies. Torsional optokinetic nystagmus (OKN) evoked by a full-field stimulus had a mean slow-phase gain of 0.22 for 10°/s drum rotation, but gain fell to 0.06 for 80°/s stimuli. Despite this fall in gain, mean OKN slow-phase velocities increased with drum speed, reaching maxima of 2.5°/s–8.0°/s in our subjects. Optokinetic afternystagmus (OKAN) was typically absent. Torsional OKN and OKAN were not modified by otolithic or proprioceptive changes caused by altering head and trunk position with respect to gravity. Torsional velocity storage is negligible in humans, regardless of head orientation.Presented in part at the Society for Neuroscience Annual Meeting, October 31, 1989, Phoenix, AZ     

The effect of muscimol micro-injections into the fastigial nucleus on the optokinetic response and the vestibulo-ocular reflex in the alert monkey

Eye movements of four macaque monkeys were investigated after unilateral micro-injections of the GABA agonist muscimol (1 g in 1 l NaCl) into the caudal fastigial nucleus, i.e. the fastigial oculomotor region. Spontaneous eye movements in the dark and in the light were tested, as well as those evoked by vestibular stimulation in the dark (sinusoidal: 0.1–0.2 Hz, ±40–100 deg/s, velocity trapezoid acceleration 40 deg/s², constant velocity 120 deg/s), optokinetic stimulation (sinusoidal: 0.1–0.2 Hz, ±40–100 deg/s, constant velocity 60–100 deg/s), and visual-vestibular conflict stimulation. With these stimuli, smooth pursuit mechanisms (fast build-up of optokinetic slow phase velocity), the vestibulo-ocular reflex (VOR) and the velocity storage mechanism were investigated. Muscimol injections consistently led to specific eye movement changes which were maximal 30–60 min after the injection and lasted 4–6 h. The fast initial rise of OKN slow phase velocity to the contralateral side decreased by 45% (range 24%–82%) of its pre-injection value, while it was virtually unaltered on the ipsilateral side (average decrease of 1%, range from a decrease of 20% to an increase of 32%). For conflict ramp stimulation, the suppression of vestibular nystagmus was less (decrease of 50%, range 12–82%) towards the contralateral side while it remained unchanged on the ipsilateral side. The VOR in the dark and the velocity storage mechanism were not altered. For the latter, the slow build-up of optokinetic nystagmus velocity, the optokinetic afternystagmus (OKAN) and the time constant of decay for the vestibular nystagmus were evaluated. There was no spontaneous nystagmus in the light or dark and no gazeholding deficit. These data support evidence that the fastigial oculomotor region contributes direction-specifically to smooth pursuit mechanisms, without affecting the VOR and the velocity storage mechanism.     

Effects of diazepam on closed- and open-loop optokinetic nystagmus (OKN) in humans

The effects of diazepam on optokinetic nystagmus (OKN) eye movements were studied under closed-loop and open-loop conditions in healthy humans. The open-loop condition was achieved by adding the eye-movement velocity signal of OKN to the computer-generated signal controlling the moving stimulus grating. Each of four subjects received a single oral dose of 5 mg diazepam or a placebo on two separate days in a double-blind randomized fashion. OKN eye movements were measured 90 min after administration of the treatments. As compared to placebo, diazepam significantly reduced the gain of open-loop OKN, but did not modify the gain of closed-loop OKN. The results indicate that the OKN gain under the open-loop condition is a more sensitive detector of the parameter changes of the OKN system than under the closed-loop condition. Thus, open-loop OKN gain can provide an objective, quantitative measure of benzodiazepine agonist effects.     

Longterm impairment of cat optokinetic nystagmus following visual cortical lesions

Summary Binocular and monocular gain of optokinetic nystagmus (OKN), OKN dynamics, vestibulo-ocular reflex (VOR) and VOR adaptation were measured in 5 normal cats and in 5 cats which underwent bilateral visual cortical lesions involving the 17–18 complex at least 4 months before testing. We observed longterm deficits after bilateral lesions involving area 17 and variable parts of area 18 but failed to observe deficits after 18–19 lesions. These deficits were limited to the OKN gain and the build-up time constant of OKN; the VOR and the optokinetic after-nystagmus (OKAN) time constant were within normal limits. Our results suggest that areas 17–18 operate in parallel to control the encoding of retinal slip velocity at the level of the nucleus of the optic tract (NOT) and the accessory optic system (AOS), which are known to represent the initial stage of the optokinetic pathways.     

The horizontal optokinetic nystagmus in the cat

Summary 1)Horizontal optokinetic eye nystagmus (OKN) and afternystagmus (OKAN) were recorded in the alert cat (head restrained) in response to velocity steps and sinusoidal optokinetic stimuli. 2)A strong dependency of OKN performance on stimulus pattern was found: responses were most regular and gain was high over a large range of stimulus velocities when the stimulus consisted of a high-contrast random dot pattern. 3) Following velocity steps, OKN showed a small amplitude fast rise in slow phase velocity (SPV) which was followed by a slow build-up to steady state. The amplitude of the initial jump in SPV increased with stimulus amplitude up to 30°/s and saturated afterwards. The plateau level of initial SPV ranged from 5 to 15°/s. 4) The slow build-up of SPV showed non-linearities, i.e. the time to steady state increased with stimulus amplitude and the slow rise of SPV was irregular. In most animals steady state SPV showed no signs of response saturation for step amplitudes up to 60–80°/s or more. The open-loop gain (steady state SPV/ retinal slip velocity) dependend on retinal slip velocity and decreased from 46 at 0.5°/s to 0.4 at about 60°/s. 5) OKAN I and II were consistently observed and occasionally OKAN III was noted. OKAN I durations (mean 13.8 +- 5.1 s) and OKAN II amplitudes were independent of stimulus magnitude. Initial SPV of OKAN I was typically the same as that of OKN, i.e. no fast fall was observed. Cessation of pattern rotation in light, however, produced a fast initial decay of SPV. 6) A least square fitting of OKAN time course was performed with various time functions. The SPV of OKAN I and II was best fitted with a damped sine wave, indicating that cat optokinetic system behaves like a second order underdamped system. 7) Sinusoidal stimuli produced strong response non-linearities. At a given frequency gain decreased with increasing stimulus amplitudes. Gain correlated best with stimulus acceleration. In addition, strong stimuli produced characteristic response distortions. 8) In the visual-vestibular conflict situation vectorial summation of VOR and OKN was observed only with small stimuli.Supported by grants nos. 3.505.79 and 3.403.83 from the Swiss National Science Foundation and Dr. Erik Slack-Gyr Foundation     

Alternating optokinetic nystagmus (OKN) induced by intermittent display of stationary gratings

In this paper, we report a novel optokinetic nystagmus (OKN), which was evoked by stationary gratings presented intermittently. OKN eye movements were accurately measured by the electromagnetic scleral search-coil technique. For the luminance stimuli, alternating OKN was elicited when the interstimulus interval (ISI) ranged from 33 to 83 ms duration and the ISI luminance approximated to the mean luminance of the stimulus grating; for chromatic (red/green) stimuli, the OKN could be evoked in non-isoluminant condition and vanished in the isoluminant condition. It is a plausible explanation that the present OKN, intermittent display-of-gratings-induced OKN (IDG-OKN), might be related to the temporal impulse response of the luminance channel in vision.     

Neuronal substrates of motor learning in the velocity storage generated during optokinetic stimulation in the squirrel monkey

Chronic motor learning in the vestibuloocular reflex (VOR) results in changes in the gain of this reflex and in other eye movements intimately associated with VOR behavior, e.g., the velocity storage generated by optokinetic stimulation (OKN velocity storage). The aim of the present study was to identify the plastic sites responsible for the change in OKN velocity storage after chronic VOR motor learning. We studied the neuronal responses of vertical eye movement flocculus target neurons (FTNs) during the optokinetic after-nystagmus (OKAN) phase of the optokinetic response (OKR) before and after VOR motor learning. Our findings can be summarized as follows. 1) Chronic VOR motor learning changes the horizontal OKN velocity storage in parallel with changes in VOR gain, whereas the vertical OKN velocity storage is more complex, increasing with VOR gain increases, but not changing following VOR gain decreases. 2) FTNs contain an OKAN signal having opposite directional preferences after chronic high versus low gain learning, suggesting a change in the OKN velocity storage representation of FTNs. 3) Changes in the eye-velocity sensitivity of FTNs during OKAN are correlated with changes in the brain stem head-velocity sensitivity of the same neurons. And 4) these changes in eye-velocity sensitivity of FTNs during OKAN support the new behavior after high gain but not low gain learning. Thus we hypothesize that the changes observed in the OKN velocity storage behavior after chronic learning result from changes in brain stem pathways carrying head velocity and OKN velocity storage information, and that a parallel pathway to vertical FTNs changes its OKN velocity storage representation following low, but not high, gain VOR motor learning.     

Optokinetic and vestibulo-ocular reflexes in dark-reared rabbits

Summary Rabbits were raised in complete darkness for 7 months after birth. Eye movements were measured at the end of this period and in the next 3 months of normal light exposure with chronically implanted scleral coils. Horizontal optokinetic nystagmus (OKN) was tested inside a large drum which was rotated at velocities between 0.06 and 60 °/sec. Vestibuloocular reflexes (VOR) were elicited by sinusoidal horizontal oscillation on a torsion swing at frequencies between 0.11 and 2.13 Hz and amplitudes up to 10 °. At the end of the light-deprived period (with the eyes still covered) a VOR could be elicited consisting of a normal mixture of smooth and saccadic components and normal phase relations, but the amplitude of the smooth (compensatory) component was reduced to about 1/3 of normal control values. At the first exposure to light an OKN could be immediately elicited which was normal in most respects, except for a reduction of the ratio slow phase eye speed/drum speed to about 2/3 of the value in normal controls. The preference of each eye for anterior motion and the quasi-conjugate character of nystagmus in monocular stimulation were unaffected. Also the improvement of the VOR by vision was normal. No abnormal habituation or fatigeability were observed. In the next 3 months of normal light exposure about half of the amplitude defects in both systems were restored, largely in the first week. The remaining defects were apparently permanent.