Monocular Optokinetic Nystagmus Research Articles

Comparison of Naso-temporal Asymmetry During Monocular Smooth Pursuit, Optokinetic Nystagmus, and Ocular Following Response in Strabismic Monkeys

ABSTRACTPurpose: Under monocular viewing conditions, humans and monkeys with infantile strabismus exhibit asymmetric naso-temporal (N-T) responses to motion stimuli. The goal of this study was to compare and contrast these N-T asymmetries during 3 visually mediated eye tracking tasks—optokinetic nystagmus (OKN), smooth pursuit (SP) response, and ocular following responses (OFR). Methods: Two adult strabismic monkeys were tested under monocular viewing conditions during OKN, SP, or OFR stimulation. OKN stimulus was unidirectional motion of a 30°x30° random dot pattern at 20°, 40°, or 80°/s for 1 minute. OFR stimulus was brief (200 ms) unidirectional motion of a 38°x28°whitenoise at 20°, 40°, or 80°/s. SP stimulus consisted of foveal step-ramp target motion at 10°, 20°, or 40°/s. Results: Mean nasalward steady state gain (0.87±0.16) was larger than temporalward gain (0.67±0.19) during monocular OKN (P<0.001). In monocular OFR, the asymmetry is manifested as a difference in OFR velocity gain (nasalward: 0.33±0.19, temporalward: 0.22±0.12; P=0.007). During monocular SP, mean nasal gain (0.97±0.2) was larger than temporal gain (0.66±0.14; P<0.001) and the mean nasalward acceleration during pursuit initiation (156±61°/s2) was larger than temporalward acceleration (118±77°/s2; P=0.04). Comparison of N-T asymmetry ratio across the 3 conditions using ANOVA showed no significant difference. Conclusions: N-T asymmetries are identified in all 3 visual tracking paradigms in both monkeys with either eye viewing. Our data are consistent with the current hypothesis for the mechanism for N-T asymmetry that invokes an imbalance in cortical drive to brainstem circuits.

An active-efficient-coding model of optokinetic nystagmus.

Optokinetic nystagmus (OKN) is an involuntary eye movement responsible for stabilizing retinal images in the presence of relative motion between an observer and the environment. Fully understanding the development of OKN requires a neurally plausible computational model that accounts for the neural development and the behavior. To date, work in this area has been limited. We propose a neurally plausible framework for the joint development of disparity and motion tuning in the visual cortex and of optokinetic and vergence eye-movement behavior. To our knowledge, this framework is the first developmental model to describe the emergence of OKN in a behaving organism. Unlike past models, which were based on scalar models of overall activity in different neural areas, our framework models the development of the detailed connectivity both from the retinal input to the visual cortex and from the visual cortex to the motor neurons. This framework accounts for the importance of the development of normal vergence control and binocular vision in achieving normal monocular OKN behaviors. Because the model includes behavior, we can simulate the same perturbations as past experiments, such as artificially induced strabismus. The proposed model agrees both qualitatively and quantitatively with a number of findings from the literature on both binocular vision and the optokinetic reflex. Finally, our model makes quantitative predictions about OKN behavior using the same methods used to characterize OKN in the experimental literature.

Object-selective responses evoked by phase-shift motion stimuli in macaque inferior temporal cortex: A case study using chronically implanted multielectrode arrays

In frogs, the horizontal monocular optokinetic nystagmus (OKN) is asymmetrical, with only the temporal-nasal (T-N) stimulation being efficient to evoke the reflex. Coil recordings showed that, in adult animals, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component. A unique microinjection of GABAA agonist THIP or of muscarinic antagonist atropine into the nucleus lentiformis mesencephali (nLM), the pretectal mesencephalic structure involved in OKN, transiently abolished the presence of the N-T component. Daily microinjections of the NMDA antagonist APV into the nLM, during the week of monocular deprivation, prevented the appearance of the N-T component. The results suggest that this phenomenon of visual plasticity can be due to reduction in pretectal GABAergic inhibition, and to concomitant activation of both cholinergic muscarinic and NMDA receptors.

Optokinetic nystagmus in strabismus: are asymmetries related to binocularity?

Strabismus may be associated with an asymmetry of monocular horizontal optokinetic nystagmus (OKN). It is unclear whether OKN asymmetries are associated with deficiency in binocular and/or stereovision. In the current study, patients with different degrees of binocularity were investigated. OKN was examined in the dominant and nondominant eyes of four groups of patients: (1) no measurable binocularity (NB), (2) poor binocularity (PB)-that is, showing binocularity on the Bagolini Test and/or rudimentary stereovision, (3) good binocularity (GB) with good stereoacuity after squint surgery, and (4) a control group. Monocular OKN was elicited with black-and-white stripes moving temporally to nasally (TN) or nasally to temporally (NT) at velocities of 15, 30, 45, and 60 deg/s. Eye movements were recorded with infrared oculography. Only subjects in the NB group showed a significant OKN asymmetry, with preference for TN stimulation in dominant and nondominant eyes. Subjects with PB did not have significant OKN asymmetries but reduced OKN gains in both stimulus directions. Subjects with GB had normal mean OKN gains without asymmetry. Larger OKN asymmetries were correlated with younger age at detection of strabismus if NB and GB were grouped together, but not if each group was analyzed separately. For the first time, a large groups of patients classified by level of binocular vision has been investigated. The results show that OKN gain and asymmetry are associated with the development of binocular vision. OKN investigation may be helpful to identify patients with binocularity or binocular potential in strabismus.

Characteristics of glucose metabolism in the visual cortex of amblyopes using positron-emission tomography and statistical parametric mapping.

The effects of amblyopia on the glucose metabolism in the visual cortex in the resting state are evaluated, the asymmetry of glucose metabolism in the ipsilateral and the contralateral occipital lobes was examined by comparing the number of hypometabolic pixels in both occipital lobes, and the correlation between this asymmetry and the results of the ophthalmologic tests was evaluated. Eleven amblyopes (7 anisometropic and 4 strabismic) and 12 normal subjects were studied with their eyes open, but without any further visual stimulus using F-18-fluorodeoxyglucose positron-emission tomography (PET) and statistical parametric mapping. Ophthalmologic tests including stereoacuity, contrast sensitivity function, monocular optokinetic nystagmus, and visual evoked potential (VEP) were measured. Compared to normal subjects, glucose metabolism decreased in Brodmann area (BA) 17, BAs 18/19, both inferior temporal lobes (BAs 37 and 20), and the superior parietal lobe (BA 7) in amblyopic patients, regardless of strabismic or anisometropic amblyopia. The laterality index of the hypometabolic pixels in the occipital lobe closely correlated with the asymmetry in the latency time of VEP (r = 0.82, P <0.05). These results suggest that PET imaging of glucose metabolism can provide a functional mapping of the visual cortex in human amblyopia.

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.

Gaze-Stabilizing Deficits and Latent Nystagmus in Monkeys With Early-Onset Visual Deprivation: Role of the Pretectal NOT

We studied the role of the pretectal nucleus of the optic tract (NOT) in the development of monocular optokinetic nystagmus (OKN) asymmetries and latent nystagmus (LN) in two monkeys reared with binocular deprivation (BD) caused by binocular eyelid suture for either the first 25 or 55 days of life. Single-unit recordings were performed in the right and left NOT of both monkeys at 2-3 yr of age and compared with similar unit recordings in normally reared monkeys. We also examined ocular motor behavior during electrical stimulation of the NOT and during pharmacological inactivation and activation using GABA(A) agonists and antagonists. In BD animals a large proportion of NOT units was dominated by the contralateral eye, in striking contrast to normal animals where 100% of NOT units were sensitive to stimuli delivered to either eye. In the 55-day BD animal no binocularly sensitive neurons were found, while in the 25-day BD animal 60% of NOT units retained at least some binocular sensitivity. Differences in direction sensitivity were also observed in BD animals. We found that 56% of units in the 55-day BD monkey and 10% of units in the 25-day BD monkey responded preferentially to contraversive visual motion. In contrast, only 5% of the NOT units encountered in normally reared monkeys respond preferentially during contraversive visual motion, the rest were most sensitive to ipsiversive visual motion. NOT neurons of BD monkeys showed a wide range of speed sensitivities similar to that of normal monkeys. Unilateral electrical stimulation of the NOT in BD animals induced a conjugate nystagmus with slow phases directed toward the side of stimulation. When we blocked the activity of NOT units with muscimol, a potent GABA(A) agonist, LN was abolished. In contrast, LN was increased when spontaneous activity of the NOT was enhanced with bicuculline, a GABA(A) antagonist. Our results indicate that the NOT in BD monkeys plays an important role in the OKN deficits and LN generation during monocular viewing. We hypothesize that the large proportion of units dominated by the contralateral eye contribute to the development of monocular OKN asymmetries and LN.

See-saw nystagmus and congenital nystagmus identified in the non-decussating retinal-fugal fiber syndrome

Purpose The purpose of the present study was to accurately document the oculomotor misalignments and instabilities associated with the non-decussating retinal-fugal fiber syndrome, a rare inborn, isolated, achiasmatic condition. 1–3 To date, the achiasmatic syndrome described has thus far been identified in three unrelated females. 1–4 A comparable achiasmatic condition has also been identified in a canine breed. 5,6 Materials and Methods The unique, inborn visual pathway malformation in the form of an isolated absence of the optic chiasm was confirmed by metabolic assay, the visual evoked potential (VEP) misrouting paradigm and neuroradiological evaluation, including magnetic resonance imaging (MRI). Horizontal and vertical, left and right eye, oculomotor scleral search coil recordings were measured, in one of the achiasmats, at 15 years of age. Comparable oculomotor recordings were implemented in three controls, including a normal age-matched control, an adult control and an adult with idiopathic congenital nystagmus (CN). In addition to central and eccentric target fixation with binocular and monocular viewing, binocular and monocular pursuit and optokinetic nystagmus (OKN) also were recorded. Results Following a binocular and monocular fixation paradigm, classic congenital nystagmus (CN) profiles were recorded in the achiasmat in the horizontal planes together with see-saw nystagmus (SSN) in the vertical planes; an alternating esotropia and vertical tropias also were documented. The CN showed interocular conjugacy and waveforms typically exhibited well-defined foveation periods. In general, both achiasmatic horizontal and vertical eye movements as well as corresponding interocular misalignments varied with stimu-lus and recording conditions. Moreover, horizontal eye movements showed sustained interocular conjugacy while vertical eye movements typically showed disconjugacy. Previous oculomotor studies in the achiasmatic canine breed revealed comparable oculomotor instabilities, albeit the latter were reported to present primarily with unyoked eye movements and uniocular saccades. In the present study, in addition to target fixation with binocular and monocular viewing, binocular and monocular pursuit and OKN responses also were recorded. For the achiasmat, high-gain pursuit results, as with eccentric fixation, emphasized a preference for fixation with the adducting eye. Also at eccentric gaze with monocular viewing, the eye under cover showed, relative to the fixating eye, a hypodeviation concomitant with adduction and a hyperdeviation concomitant with abduction. OKN profiles in the achiasmat with stimuli presented under both normal viewing and open-loop, retinal-field locked conditions proved rather complex; however, when an OKN response was identified, reversed OKN tracking was not apparent. Conclusions In general, the oculomotor results reported herein demonstrate that the non-decussating retinal-fugal fiber syndrome is an afferent visual pathway disorder associated with vertical and horizontal misalignments concurrent with congenital nystagmus and also with the rarer see-saw nystagmus.

Monocular horizontal OKN in observers with early- and late-onset strabismus

Several reports on monocular optokinetic nystagmus (OKN) in observers with strabismus have found that asymmetry of OKN tends to occur in both eyes of observers with an early onset of strabismus but only in the deviating eye of those with a later onset of strabismus. Our objective was to quantify and compare the magnitude of the OKN asymmetry in each eye as a function of observer’s age at onset of strabismus. We studied monocular OKN in ten observers with early-onset (up to 24 months of age), seven observers with late-onset (after 24 months of age) unilateral strabismus, and 12 normally sighted control observers. In the deviating eye, observers with early-onset strabismus showed large OKN asymmetries in favour of nasalward motion while observers with late-onset strabismus showed smaller OKN asymmetries in that eye. The majority of early- and late-onset observers showed near normal OKN in the non-deviating eye although the early-onset observers showed bilateral asymmetries more often. These findings may be due to both age at onset of strabismus and chronological age and are discussed in terms of the issue of plasticity or recovery of function.

The relationship between stereopsis and monocular optokinetic nystagmus after infantile cataracts

Purpose: Visual deprivation disrupting binocular development, such as that occurring with congenital cataract, is reported to cause asymmetric monocular optokinetic nystagmus (MOKN), as well as poor sensory and motor fusional outcome. We wanted to determine if symmetric MOKN could develop in cases of congenital cataract with good fusional outcome. Methods: We tested MOKN (with video and electro-oculographic recordings) and stereoacuity on 5 patients with good visual acuity and satisfactory ocular alignment after surgery for congenital cataract. Results: Stereoacuity was better than 50 seconds of arc in 1 case of monocular cataract and 2 cases of bilateral cataract. These case patients had symmetric MOKN. In a monocular cataract case, symmetric MOKN was observed in spite of questionable stereoacuity (at least 500 arc/s). One patient showed asymmetric MOKN, despite good visual acuity, and stereoacuity of 200 arc/s. Conclusions: Patients with congenital cataract can have symmetric MOKN and good stereopsis. These cases suggest that MOKN symmetry develops along with good stereopsis, but the quality of stereopsis necessary for development of MOKN symmetry remains unclear. (J AAPOS 1999;3:221-6)

Animal models for the optokinetic system of the human

We compare the neuronal and behavioural consequences of abnormal visual experience during early infancy for the optokinetic system of cat and monkey with the neuroopthalmological results in man. Optokinetic eye movements were recorded with the search coil method and electrooculography. In addition, the response properties of single neurons in the visual cortex and pretectum of anesthetized and paralyzed cats and monkeys were determined in electrophysiological experiments. Our data show that monocular deprivation and strabismus lead to an increase of asymmetry of monocular optokinetic nystagmus and a decrease in gain of slow phase optokinetic eye movements during monocular stimulation as well as to a significant decrease of binocular convergence in the oculomotor system of both cat and monkey. Although these changes are basically similar in both species they are not identical. These differential effects may be explained by structural differences. Assuming a similar neuronal substrate for the optokinetic system in all primates the monkey represents a more suitable animal model for the human visual system than the cat.

Development of refraction and strabismus

In the past year a number of studies have provided insights into the mechanisms whereby the eye can maintain coordinated growth to achieve emmetropia. Research into factors that may lead to a failure to emmetropize also has been promising. The effect of early spectacle intervention has been debated, with some evidence from animal studies suggesting that lenses may interfere with emmetropization. Human data on this topic are limited but do not appear to show the deleterious effects of lenses reported in the animal studies. The role of early astigmatism in the emmetropization process is not clear. Myopia research continues to hold promise for the eventual discovery of treatments to slow progression. With respect to the development of strabismus, there are many mechanisms for its induction. The problem is to identify the primary ones and their interactions. This article reviews some of the newer candidates, including pulleys that affect extraocular-muscle action and the role of nasally biased monocular optokinetic nystagmus. An understanding of the critical periods of the various visual dimensions involved in the development of strabismus is also crucial.

Optokinetic reflex in squirrel monkeys after long-term monocular deprivation.

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.

Involvement of NMDA in a plasticity phenomenon observed in the adult frog monocular optokinetic nystagmus.

The frog horizontal monocular optokinetic nystagmus (H-OKN) is asymmetrical, the reflex being evoked by a temporal-nasal (T-N) component, but not by a nasal-temporal (N-T) component. Coil recordings showed that, in adult animals, 8 days of monocular deprivation (by unilateral eyelid suture) provoked the appearance of a N-T component, the H-OKN becoming symmetrical, reacting for both directions of stimulation. This delay was shortened to 2 days following two successive unilateral pretectal administrations of NMDA or of LY 285 265, an NMDA agonist, the first 2 days of eyelid suture. The same results were obtained when chronic microinjections of NMDA or LY 285 265 were achieved, the frogs being maintained in total darkness during the week of eyelid suture. These data indicate that the plasticity phenomenon evidenced in the monocular frog H-OKN depends on the activation of the NMDA receptors of one pretectum. This activation was obtained either by a monocular light stimulation of 8 days duration, or by unilateral administration of drugs activating the NMDA glutamatergic pretectal system. In this last case, the light stimulation was no longer necessary.

Monocular optokinetic nystagmus in humans with age-related maculopathy

AIMTo investigate full field monocular optokinetic nystagmus (OKN) in patients with age-related maculopathy (ARM) and relative central scotoma.METHODSSix patients aged 59–88 years with bilateral ARM and an aged-matched control group...

Single-unit responses to whole-field visual stimulation in the pretectum of Rana pipiens

Visually responsive single units were recorded from the pretectal region that includes the large-celled nucleus lentiformis mesencephali (nLM) in the leopard frog, Rana pipiens. During monocular stimulation of the contralateral eye, 60 single units responding to movement of a large-field., random-dot pattern were quantitatively analyzed using horizontal and vertical directions at each of four pattern velocities (0.4–40°/s). All units were spontaneously active, motion sensitive, and the majority showed ‘on’-‘off’ responses. Several different response profiles were observed, including velocity-sensitive units with peak response at 10°/s, most of which showed directional selectivity, and speed-sensitive units that showed increasing spike frequencies as pattern velocity increased, but little or no directional selectivity. About one-third of all units analyzed were direction-selective, and 55% of those responded optimally to the temporal-to-nasal (T-N) direction of motion. T-N units were recorded primarily from an area that lies dorsolaterally between nLM and the optic tectum, in the ‘peri-nLM’ region. The pronounced monocular optokinetic nystagmus (OKN) response asymmetry that occurs in anurans appears to be reflected in the response profiles of the T-N direction selective units.

Clinical optokinetic nystagmus asymmetry in treated esotropes.

Monocular optokinetic nystagmus (OKN) asymmetry is associated with disruption of early binocular visual development. Three groups of treated esotropic patients and a group of normal controls were evaluated for the presence of clinically detectable monocular OKN asymmetry. Clinical assessment of monocular OKN asymmetry was performed by observing eye movements in response to a hand-held rotating drum. Asymmetry was quantitated on a scale of 0 to +3 OKN asymmetry. Clinical OKN asymmetry was evaluated in the following groups of patients: those with congenital esotropia treated with very early surgery achieving high-grade stereo acuity (group 1); those with congenital esotropia treated with late surgery achieving no stereopsis (group 2); those with acquired esotropia achieving high-grade stereo acuity after treatment with spectacle correction (group 3); and normal controls (group 4). Two of the three patients in group 1 showed +3 OKN asymmetry despite having high-grade stereo acuity; the third one, who was surgically aligned earliest (13 weeks), demonstrated +1 OKN asymmetry. This patient achieved orthotropia, 40 seconds stereo acuity, perfect Randot stereo acuity, and had no dissociated vertical deviation or latent nystagmus. All 10 patients in group 2 (those with late alignment-after 1 year-and no stereo acuity) showed +3 OKN asymmetry. All four patients in group 3 (those with acquired hypermetropic esotropia and high-grade stereo acuity after treatment) and all 10 patients in the normal control group showed no OKN asymmetry. Clinically obvious monocular OKN asymmetry can occur in patients with congenital esotropia who are aligned early and develop high-grade stereo acuity. Even brief periods of strabismus during the early period of binocular motor development can result in persistent OKN asymmetry. This suggests that binocular motor processing may develop distinct from, and prior to, the development of high-grade stereo acuity. OKN asymmetry appears to be a clinical sign of an insult to early binocular motor development.

Asymmetry of motion VEP in infantile strabismus and in central vestibular nystagmus.

Norcia et al. [1] found a nasal-temporal asymmetry of visually evoked potentials (VEP) elicited by motion stimuli in patients with infantile strabismus. Patients with infantile strabismus typically present with an asymmetry of the monocular optokinetic nystagmus (OKN). We here address the question whether the asymmetry of the motion VEP indicates a sensory defect in the afferent visual pathway that could explain the OKN asymmetry. We recorded the VEP to a horizontally oscillating vertical sinusoidal grating in 20 patients with infantile strabismus (esotropia, asymmetry of the monocular optokinetic nystagmus, latent nystagmus) and in 10 normal controls. No asymmetry occurred in the 10 controls. Eight of the 20 patients with infantile strabismus showed a clear difference between the VEPs evoked by back and forth movements with a mirror-like asymmetry between the two eyes (phase shift 180 +/- 20 degrees). However, there was no significant correlation between the degree of VEP and OKN asymmetries. Therefore, we assume that the VEP asymmetry does not reflect the primary cause of the OKN asymmetry. Rather, the OKN asymmetry may be due to a sensory-motor defect in the efferent subcortical pathway, and the VEP asymmetry could be an epiphenomenon. Some of the VEP asymmetry may be a consequence of the latent nystagmus typically released under monocular stimulation, leading to adaptation of the afferent retino-cortical pathway. This suggestion is supported by a marked VEP asymmetry that we found in two patients with an acquired central vestibular nystagmus, an abnormality most likely not combined with a primary defect of the retino-cortical pathway.

Different effects of dopamine and Piribedil (a dopamine D 2 agonist) on frog monocular optokinetic nystagmus asymmetry

Frog monocular optokinetic nystagmus (OKN) displays a directional asymmetry, reacting only to stimulations in the temporal-nasal (T N) direction. The nasal-temporal (N T) component is almost absent. The systemic or intrapretectal injection of Piribedil, a D 2 dopamine agonist, provokes the appearance of a N T component suppressing the monocular OKN asymmetry. Conversely, dopamine or haloperidol (a dopamine antagonist, acting mainly on D 2 receptors) have no effect upon the monocular OKN unidirectionality. The monocular OKN N T component still appears after administration of Piribedil even if this injection is preceded by administration of haloperidol which blocks the dopaminergic D 2 receptors. Moreover administration of atropine (a cholinergic muscarinic antagonist) following that of Piribedil suppresses the N T component; when injected before Piribedil, atropine prevents the appearance of the N T component. These results suggest that in our experiments, Piribedil binds with muscarinic receptors.

Are retinal or mesencephalic dopaminergic systems involved in monocular optokinetic nystagmus asymmetry in frog?

In monocular vision, frogs display a unidirectional optokinetic horizontal nystagmus (H-OKN) reacting only to temporal-nasal (T-N) stimulation. The N-T component is almost absent. The analysis of search coil recordings after administration of dopamine into the viewing eye, the occluded eye or directly into the pretectum, hardly modifies the H-OKN triggered by the viewing eye irrespective of the concentration used. Conversely, administration of Piribedil, a strong D2 dopamine agonist, provokes the appearance of a N-T component, suppressing the monocular H-OKN asymmetry, whether the drug is injected by intravitreal or intrapretectal route. It is suggested that Piribedil could also bind with receptors other than dopamine's.