Optokinetic Nystagmus Research Articles

Eye Movement Abnormalities in Glaucoma Patients: A Review.

Glaucoma is a common condition that relies on careful clinical assessment to diagnose and determine disease progression. There is growing evidence that glaucoma is associated not only with loss of retinal ganglion cells but also with degeneration of cortical and subcortical brain structures associated with vision and eye movements. The effect of glaucoma pathophysiology on eye movements is not well understood. In this review, we examine the evidence surrounding altered eye movements in glaucoma patients compared to healthy controls, with a focus on quantitative eye tracking studies measuring saccades, fixation, and optokinetic nystagmus in a range of visual tasks. The evidence suggests that glaucoma patients have alterations in several eye movement domains. Patients exhibit longer saccade latencies, which worsen with increasing glaucoma severity. Other saccadic abnormalities include lower saccade amplitude and velocity, and difficulty inhibiting reflexive saccades. Fixation is pathologically altered in glaucoma with reduced stability. Optokinetic nystagmus measures have also been shown to be abnormal. Complex visual tasks (eg reading, driving, and navigating obstacles), integrate these eye movements and result in behavioral adaptations. The review concludes with a summary of the evidence and recommendations for future research in this emerging field.

CerebelluMorphic: Large-Scale Neuromorphic Model and Architecture for Supervised Motor Learning.

The cerebellum plays a vital role in motor learning and control with supervised learning capability, while neuromorphic engineering devises diverse approaches to high-performance computation inspired by biological neural systems. This article presents a large-scale cerebellar network model for supervised learning, as well as a cerebellum-inspired neuromorphic architecture to map the cerebellar anatomical structure into the large-scale model. Our multinucleus model and its underpinning architecture contain approximately 3.5 million neurons, upscaling state-of-the-art neuromorphic designs by over 34 times. Besides, the proposed model and architecture incorporate 3411k granule cells, introducing a 284 times increase compared to a previous study including only 12k cells. This large scaling induces more biologically plausible cerebellar divergence/convergence ratios, which results in better mimicking biology. In order to verify the functionality of our proposed model and demonstrate its strong biomimicry, a reconfigurable neuromorphic system is used, on which our developed architecture is realized to replicate cerebellar dynamics during the optokinetic response. In addition, our neuromorphic architecture is used to analyze the dynamical synchronization within the Purkinje cells, revealing the effects of firing rates of mossy fibers on the resonance dynamics of Purkinje cells. Our experiments show that real-time operation can be realized, with a system throughput of up to 4.70 times larger than previous works with high synaptic event rate. These results suggest that the proposed work provides both a theoretical basis and a neuromorphic engineering perspective for brain-inspired computing and the further exploration of cerebellar learning.

Cortical mechanisms of visual brightness.

SUMMARYThe primary visual cortex signals the onset of light and dark stimuli with ON and OFF cortical pathways. Here, we demonstrate that both pathways generate similar response increments to large homogeneous surfaces and their response average increases with surface brightness. We show that, in cat visual cortex, response dominance from ON or OFF pathways is bimodally distributed when stimuli are smaller than one receptive field center but unimodally distributed when they are larger. Moreover, whereas small bright stimuli drive opposite responses from ON and OFF pathways (increased versus suppressed activity), large bright surfaces drive similar response increments. We show that this size-brightness relation emerges because strong illumination increases the size of light surfaces in nature and both ON and OFF cortical neurons receive input from ON thalamic pathways. We conclude that visual scenes are perceived as brighter when the average response increments from ON and OFF cortical pathways become stronger.

Effect of Green Tea and Tea Catechin on the Visual Motion Processing for Optokinetic Responses in Mice

In general, catechins contained in green tea are believed to have positive effects on the human body and mental health. The intake of epigallocatechin gallate (EGCG), a major polyphenol in green tea, is known to be effective for retinal protection; however, whether green tea and/or EGCG affect visual function remains unknown. In the present study, we investigated the effect of green tea and EGCG on visual motion processing by measuring optokinetic responses (OKRs) in young adult and aging mice. Young and aging mice (C57BL6/J) were fed a control diet (control) or the test diet, which contained matcha green tea powder or green tea extract (dried sencha green tea infusion), for 1 month, and their OKRs were measured. They were then intraperitoneally administered saline (control) or EGCG, and OKRs were measured. We found that the OKRs of young and aging mice after green tea intake and after EGCG administration showed higher temporal sensitivity than those of control mice. The visual ability to detect moving objects was enhanced in young and aging mice upon intake of green tea or EGCG. From the above results, the visual motion processing for optokinetic responses by ingesting green tea was enhanced, which may be related to the effect of EGCG.

Homeostatic plasticity of eye movement performance in Xenopus tadpoles following prolonged visual image motion stimulation

Visual image motion-driven ocular motor behaviors such as the optokinetic reflex (OKR) provide sensory feedback for optimizing gaze stability during head/body motion. The performance of this visuo-motor reflex is subject to plastic alterations depending on requirements imposed by specific eco-physiological or developmental circumstances. While visuo-motor plasticity can be experimentally induced by various combinations of motion-related stimuli, the extent to which such evoked behavioral alterations contribute to the behavioral demands of an environment remains often obscure. Here, we used isolated preparations of Xenopus laevis tadpoles to assess the extent and ontogenetic dependency of visuo-motor plasticity during prolonged visual image motion. While a reliable attenuation of large OKR amplitudes can be induced already in young larvae, a robust response magnitude-dependent bidirectional plasticity is present only at older developmental stages. The possibility of older larvae to faithfully enhance small OKR amplitudes coincides with the developmental maturation of inferior olivary–Purkinje cell signal integration. This conclusion was supported by the loss of behavioral plasticity following transection of the climbing fiber pathway and by the immunohistochemical demonstration of a considerable volumetric extension of the Purkinje cell dendritic area between the two tested stages. The bidirectional behavioral alterations with different developmental onsets might functionally serve to standardize the motor output, comparable to the known differential adaptability of vestibulo-ocular reflexes in these animals. This homeostatic plasticity potentially equilibrates the working range of ocular motor behaviors during altered visuo-vestibular conditions or prolonged head/body motion to fine-tune resultant eye movements.

Conserved subcortical processing in visuo-vestibular gaze control

Gaze stabilization compensates for movements of the head or external environment to minimize image blurring. Multisensory information stabilizes the scene on the retina via the vestibulo-ocular (VOR) and optokinetic (OKR) reflexes. While the organization of neuronal circuits underlying VOR is well-described across vertebrates, less is known about the contribution and evolution of the OKR and the basic structures allowing visuo-vestibular integration. To analyze these neuronal pathways underlying visuo-vestibular integration, we developed a setup using a lamprey eye-brain-labyrinth preparation, which allowed coordinating electrophysiological recordings, vestibular stimulation with a moving platform, and visual stimulation via screens. Lampreys exhibit robust visuo-vestibular integration, with optokinetic information processed in the pretectum that can be downregulated from tectum. Visual and vestibular inputs are integrated at several subcortical levels. Additionally, saccades are present in the form of nystagmus. Thus, all basic components of the visuo-vestibular control of gaze were present already at the dawn of vertebrate evolution.

A New Optokinetic Testing Method to Measure Rat Vision.

Optokinetic nystagmus (OKN) is a reflexive eye movement initiated by the motion of visual stimuli in the field of vision. The head-tracking movement associated with OKN is commonly used as a measure of visual function in rodents. To record OKN responses in normal and experimental rats, a simple and inexpensive apparatus has been developed. This setup uses two tablet screens to display the OKN visual stimulus consisting of high contrast black and white stripes generated using the OKN Stripes Visualization Web Application, a freely available software. The rat is placed inside a clear Plexiglass holder that limitsmovement so that therat's head continuously faces the OKN display screen. The position of the rat holder can be changed to adjust the distance between the rat and the display screen. A micro-camera positioned above the rat holder is used to record the rat's visual activities. These recordings can be used for quantitative assessments. Based on the presence or absence of clear head-tracking, the OKN responses at different spatial frequencies can be determined. The collected data demonstrates a novel technique for reliable measurement of visual acuity in normal and retinal degenerate rats.

Adaptation of Optokinetic Reflex by Training with Different Frequency and Amplitude.

Although the occurrence of optokinetic reflex (OKR) adaptation after OKR training is well established, the dynamic properties of OKR adaptation has not been fully studied. This study aimed to examine the difference in the amount of OKR adaptation according to OKR training protocols which have different frequency or amplitude of drum oscillation. Using C57BL/6N male mice, we induced OKR adaptation by 3 different categories of learning paradigm as follows: (1) Optokinetic drum oscillation for 60 min with same amplitude and different frequency. (2) Optokinetic drum oscillation for 60 min with same frequency and different amplitude. (3) Training with serial combination of different frequency or amplitude. The results show that the amount of OKR adaptation was greater after OKR training with lower frequency or amplitude than that with higher frequency or amplitude. This finding may suggest that the retinal slip signal with lower-velocity OKR stimulation serves as more precise instructive signal for learning, leading to induction of more efficient training effect. Another interesting finding was that the OKR gain increase tended to be greater after training composed of sequential combination of decreasing frequency or amplitude than that composed of sequential combination of increasing frequency or amplitude. Furthermore, the OKR training with high frequency or amplitude eliminated a part of learning effects which have already formed by previous training. We postulate that the stimulation during training with high frequency or amplitude may implement a disturbing instruction for OKR learning when it is conducted in mice with increased OKR gain after previous OKR training.

Increased Reliability of Visually-Evoked Activity in Area V1 of the MECP2-Duplication Mouse Model of Autism.

Atypical sensory processing is now thought to be a core feature of the autism spectrum. Influential theories have proposed that both increased and decreased neural response reliability within sensory systems could underlie altered sensory processing in autism. Here, we report evidence for abnormally increased reliability of visual-evoked responses in layer 2/3 neurons of adult male and female primary visual cortex in the MECP2-duplication syndrome animal model of autism. Increased response reliability was due in part to decreased response amplitude, decreased fluctuations in endogenous activity, and an abnormal decoupling of visual-evoked activity from endogenous activity. Similar to what was observed neuronally, the optokinetic reflex occurred more reliably at low contrasts in mutant mice compared with controls. Retinal responses did not explain our observations. These data suggest that the circuit mechanisms for combining sensory-evoked and endogenous signal and noise processes may be altered in this form of syndromic autism.SIGNIFICANCE STATEMENT Atypical sensory processing is now thought to be a core feature of the autism spectrum. Influential theories have proposed that both increased and decreased neural response reliability within sensory systems could underlie altered sensory processing in autism. Here, we report evidence for abnormally increased reliability of visual-evoked responses in primary visual cortex of the animal model for MECP2-duplication syndrome, a high-penetrance single-gene cause of autism. Visual-evoked activity was abnormally decoupled from endogenous activity in mutant mice, suggesting in line with the influential "hypo-priors" theory of autism that sensory priors embedded in endogenous activity may have less influence on perception in autism.

Deficiency of protocadherin 9 leads to reduction in positive emotional behaviour

Protocadherin 9 (Pcdh9) is a member of the cadherin superfamily and is uniquely expressed in the vestibular and limbic systems; however, its physiological role remains unclear. Here, we studied the expression of Pcdh9 in the limbic system and phenotypes of Pcdh9-knock-out mice (Pcdh9 KO mice). Pcdh9 mRNA was expressed in the fear extinction neurons that express protein phosphatase 1 regulatory subunit 1 B (Ppp1r1b) in the posterior part of the basolateral amygdala (pBLA), as well as in the Cornu Ammonis (CA) and Dentate Gyrus (DG) neurons of the hippocampus. We show that the Pcdh9 protein was often localised at synapses. Phenotypic analysis of Pcdh9 KO mice revealed no apparent morphological abnormalities in the pBLA but a decrease in the spine number of CA neurons. Further, the Pcdh9 KO mice were related to features such as the abnormal optokinetic response, less approach to novel objects, and reduced fear extinction during recovery from the fear. These results suggest that Pcdh9 is involved in eliciting positive emotional behaviours, possibly via fear extinction neurons in the pBLA and/or synaptic activity in the hippocampal neurons, and normal optokinetic eye movement in brainstem optokinetic system-related neurons.

An Effective Algorithm to Analyze the Optokinetic Nystagmus Waveforms from a Low-Cost Eye Tracker.

Objective: Most neurological diseases are usually accompanied by changes in the oculomotor nerve. Analysis of different types of eye movements will help provide important information in ophthalmology, neurology, and psychology. At present, many scholars use optokinetic nystagmus (OKN) to study the physiological phenomenon of eye movement. OKN is an involuntary eye movement induced by a large moving surrounding visual field. It consists of a slow pursuing eye movement, called “slow phase” (SP), and a fast re-fixating saccade eye movement, called “fast phase” (FP). Non-invasive video-oculography has been used increasingly in eye movement research. However, research-grade eye trackers are often expensive and less accessible to most researchers. Using a low-cost eye tracker to quantitatively measure OKN eye movement will facilitate the general application of eye movement research. Methods & Results: We design an analytical algorithm to quantitatively measure OKN eye movements on a low-cost eye tracker. Using simple conditional filtering, accurate FP positions can be obtained quickly. The high-precision FP recognition rate is of great help for the subsequent calculation of eye movement analysis parameters, such as mean slow phase velocity (MSPV), which is beneficial as a reference index for patients with strabismus and other eye diseases. Conclusions: Experimental results indicate that the proposed method achieves faster and better results than other approaches, and can provide an effective algorithm to calculate and analyze the FP position of OKN waveforms.

Impact of walking speed and motion adaptation on optokinetic nystagmus-like head movements in the blowfly Calliphora

The optokinetic nystagmus is a gaze-stabilizing mechanism reducing motion blur by rapid eye rotations against the direction of visual motion, followed by slower syndirectional eye movements minimizing retinal slip speed. Flies control their gaze through head turns controlled by neck motor neurons receiving input directly, or via descending neurons, from well-characterized directional-selective interneurons sensitive to visual wide-field motion. Locomotion increases the gain and speed sensitivity of these interneurons, while visual motion adaptation in walking animals has the opposite effects. To find out whether flies perform an optokinetic nystagmus, and how it may be affected by locomotion and visual motion adaptation, we recorded head movements of blowflies on a trackball stimulated by progressive and rotational visual motion. Flies flexibly responded to rotational stimuli with optokinetic nystagmus-like head movements, independent of their locomotor state. The temporal frequency tuning of these movements, though matching that of the upstream directional-selective interneurons, was only mildly modulated by walking speed or visual motion adaptation. Our results suggest flies flexibly control their gaze to compensate for rotational wide-field motion by a mechanism similar to an optokinetic nystagmus. Surprisingly, the mechanism is less state-dependent than the response properties of directional-selective interneurons providing input to the neck motor system.

Astaxanthin Ameliorates Diabetic Retinopathy in Swiss Albino Mice via Inhibitory Processes of Neuron-Specific Enolase Activity

Retinopathy is one of the most common complications of diabetes mellitus. Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabetic properties. However, the therapeutic effect of AST on DR remains elusive. The present study is designed to investigate the effects of AST on DR via inhibition of neuron-specific enolase (NSE) activity. DR was induced by the administration of streptozotocin (STZ, 35 mg/kg: intraperitoneal; and 20 μL of STZ: intravitreal) in mice. AST (10 and 20 mg/kg) was administered orally (p.o.) for 21 days. The DR associated visual changes were assessed at different time intervals via optokinetic motor response (OMR) and penta-maze (PM) tests. Blood glucose level as well as retinal catalase, lactate dehydrogenase (LDH), & neuron-specific enolase (NSE) were estimated. The reference drug i.e., dexamethasone (DEX, 10 mg/kg; p.o.) was administered for 21 days. The administration of AST showed significant ameliorative potential in DR. Hence, AST can be used as a natural medicine for the management of DR due to its potential antioxidant, anti-diabetic, and NSE inhibitory properties.

Quantitative assessment of oculomotor function by videonystagmography in multiple system atrophy

ObjectiveTo quantitatively assess oculomotor impairments in multiple system atrophy (MSA) and to explore their correlation with clinical characteristics. MethodsWe recruited 45 patients with MSA, including 21 with dominant ataxia (MSA-C), 24 with dominant parkinsonism (MSA-P), and 40 age-matched healthy controls. Detailed oculomotor performance in the horizontal direction was measured using videonystagmography (VNG). ResultsWe found that the proportion of abnormal eye movements in patients with MSA was 93.3% (37.7%, 51.1%, 73.3%, 71.1%, and 37.8% on fixation and gaze-holding, without fixation, saccade, smooth pursuit, and optokinetic nystagmus tests, respectively). Patients with MSA-C showed significantly lower gains in smooth pursuit test and optokinetic nystagmus test, and a higher incidence of hypermetria in the saccade test than patients with MSA-P (all P < 0.05). No oculomotor deficits were correlated with age, age of onset, sex, disease duration, or Unified Multiple System Atrophy Rating Scale (USMARS) (all r < 0.25, P > 0.1). ConclusionsAn extremely high incidence of oculomotor impairments could be observed using VNG in both the MSA-C and MSA-P subtypes, although there were some differences between them. SignificanceA comprehensive oculomotor examination could serve as a valuable tool in the diagnostic workup of patients with MSA.

Oculomotor abnormalities and its association with sleep stages in progressive supranuclear palsy

BackgroundOculomotor abnormalities are one of the cardinal clinical features of progressive supranuclear palsy (PSP). Vertical saccadic slowing is an early sign of PSP. The association between oculomotor abnormalities and sleep architecture has not been studied so far. ObjectivesTo study the association of oculomotor abnormalities of PSP with the sleep stages by using video polysomnography (vPSG). MethodsThis was a cross-sectional single-center study. Twenty-two patients with PSP and 15 age and gender-matched controls were recruited. Saccades, vestibulo-ocular reflex, and optokinetic nystagmus were assessed and graded clinically in all patients and one overnight vPSG was done in all cases. ResultsVertical saccades, upward more than downwards, were affected in all cases. While horizontal saccades were normal only in 41% of cases. Vertical optokinetic nystagmus (OKN) was affected in all cases. Horizontal OKN was normal in 36% of patients. The vertical upward saccades had a negative correlation with N1% and duration (r = −0.418; p = 0.05, r = −0.457; p = 0.03), N3% and duration (r = −0.486; p = 0.02, r = −0.510; p = 0.01), REM% (r = −0.449; p = 0.04), total sleep time (r = −0.487; p = 0.02) and sleep efficiency (r = −0.444; p = 0.04). There was a positive correlation between horizontal OKN and sleep onset latency (r = 0.432; p = 0.05). ConclusionsVertical saccadic restriction in PSP has significant negative correlation with total sleep time and sleep efficiency. The oculomotor and sleep abnormalities in PSP are probably interlinked and their assessment is useful in determining the characteristics of the disease.

Selective Upregulation of SIRT1 Expression in Retinal Ganglion Cells by AAV-Mediated Gene Delivery Increases Neuronal Cell Survival and Alleviates Axon Demyelination Associated with Optic Neuritis.

Optic neuritis (ON), the most common ocular manifestation of multiple sclerosis, is an autoimmune inflammatory demyelinating disease also characterized by degeneration of retinal ganglion cells (RGCs) and their axons, which commonly leads to visual impairment despite attempted treatments. Although ON disease etiology is not known, changes in the redox system and exacerbated optic nerve inflammation play a major role in the pathogenesis of the disease. Silent information regulator 1 (sirtuin-1/SIRT1) is a ubiquitously expressed NAD+-dependent deacetylase, which functions to reduce/prevent both oxidative stress and inflammation in various tissues. Non-specific upregulation of SIRT1 by pharmacologic and genetic approaches attenuates RGC loss in experimental ON. Herein, we hypothesized that targeted expression of SIRT1 selectively in RGCs using an adeno-associated virus (AAV) vector as a delivery vehicle is an effective approach to reducing neurodegeneration and preserving vision in ON. We tested this hypothesis through intravitreal injection of AAV7m8.SNCG.SIRT1, an AAV2-derived vector optimized for highly efficient SIRT1 transgene transfer and protein expression into RGCs in mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis that recapitulates optic neuritis RGC loss and axon demyelination. Our data show that EAE mice injected with a control vehicle exhibit progressive alteration of visual function reflected by decreasing optokinetic response (OKR) scores, whereas comparatively, AAV7m8.SNCG.SIRT1-injected EAE mice maintain higher OKR scores, suggesting that SIRT1 reduces the visual deficit imparted by EAE. Consistent with this, RGC survival determined by immunolabeling is increased and axon demyelination is decreased in the AAV7m8.SNCG.SIRT1 RGC-injected group of EAE mice compared to the mouse EAE counterpart injected with a vehicle or with control vector AAV7m8.SNCG.eGFP. However, immune cell infiltration of the optic nerve is not significantly different among all EAE groups of mice injected with either vehicle or AAV7m8.SNCG.SIRT1. We conclude that despite minimally affecting the inflammatory response in the optic nerve, AAV7m8-mediated SIRT1 transfer into RGCs has a neuroprotective potential against RGC loss, axon demyelination and vison deficits associated with EAE. Together, these data suggest that SIRT1 exerts direct effects on RGC survival and function.

Localization of long-term synaptic plasticity defects in cerebellar circuits using optokinetic reflex learning profile

Objective. Functional maps of the central nervous system attribute the coordination and control of many body movements directly or indirectly to the cerebellum. Despite this general picture, there is little information on the function of cerebellar neural components at the circuit level. The presence of multiple synaptic junctions and the synergistic action of different types of plasticity make it virtually difficult to determine the distinct contribution of cerebellar neural processes to behavioral manifestations. In this study, investigating the effect of long-term synaptic changes on cerebellar motor learning, we intend to provide quantitative criteria for localizing defects in the major forms of synaptic plasticity in the cerebellum. Approach. To this end, we develop a firing rate model of the cerebellar circuits to simulate learning of optokinetic reflex (OKR), one of the most well-known cerebellar-dependent motor tasks. In the following, by comparing the simulated OKR learning profile for normal and pathosynaptic conditions, we extract the learning features affected by long-term plasticity disorders. Next, conducting simulation with different massed (continuous with no rest) and spaced (interleaved with rest periods) learning paradigms, we estimate the detrimental impact of plasticity defects at corticonuclear synapses on short- and long-term motor memory. Main results. Our computational approach predicts a correlation between location and grade of the defect with some learning factors such as the rate of formation and retention of motor memory, baseline performance, and even cerebellar motor reserve capacity. Further, spacing analysis reveal the dependence of learning paradigm efficiency on the spatiotemporal characteristic of defect in the network. Indeed, defects in cortical memory formation and nuclear memory consolidation mainly harm massed and spaced learning, respectively. This result is used to design a differential assay for identifying the faulty phases of cerebellar learning. Significance. The proposed computational framework can help develop neural-screening systems and prepare meso-scale functional maps of the cerebellar circuits.

Loss of slc39a14 causes simultaneous manganese hypersensitivity and deficiency in zebrafish.

ABSTRACTManganese neurotoxicity is a hallmark of hypermanganesemia with dystonia 2, an inherited manganese transporter defect caused by mutations in SLC39A14. To identify novel potential targets of manganese neurotoxicity, we performed transcriptome analysis of slc39a14−/− mutant zebrafish that were exposed to MnCl2. Differentially expressed genes mapped to the central nervous system and eye, and pathway analysis suggested that Ca2+ dyshomeostasis and activation of the unfolded protein response are key features of manganese neurotoxicity. Consistent with this interpretation, MnCl2 exposure led to decreased whole-animal Ca2+ levels, locomotor defects and changes in neuronal activity within the telencephalon and optic tectum. In accordance with reduced tectal activity, slc39a14−/− zebrafish showed changes in visual phototransduction gene expression, absence of visual background adaptation and a diminished optokinetic reflex. Finally, numerous differentially expressed genes in mutant larvae normalised upon MnCl2 treatment indicating that, in addition to neurotoxicity, manganese deficiency is present either subcellularly or in specific cells or tissues. Overall, we assembled a comprehensive set of genes that mediate manganese-systemic responses and found a highly correlated and modulated network associated with Ca2+ dyshomeostasis and cellular stress. This article has an associated First Person interview with the first author of the paper.

A robust receptive field code for optic flow detection and decomposition during self-motion

The perception of optic flow is essential for any visually guided behavior of a moving animal. To mechanistically predict behavior and understand the emergence of self-motion perception in vertebrate brains, it is essential to systematically characterize the motion receptive fields (RFs) of optic-flow-processing neurons. Here, we present the fine-scale RFs of thousands of motion-sensitive neurons studied in the diencephalon and the midbrain of zebrafish. We found neurons that serve as linear filters and robustly encode directional and speed information of translation-induced optic flow. These neurons are topographically arranged in pretectum according to translation direction. The unambiguous encoding of translation enables the decomposition of translational and rotational self-motion information from mixed optic flow. In behavioral experiments, we successfully demonstrated the predicted decomposition in the optokinetic and optomotor responses. Together, our study reveals the algorithm and the neural implementation for self-motion estimation in a vertebrate visual system.

Diagnosis of colour vision deficits using eye movements

We set out to develop a simple objective test of functional colour vision based on eye movements made in response to moving patterns. We exploit the finding that while the motion of a colour-defined stimulus can be cancelled by adding a low-contrast luminance-defined stimulus moving in the opposite direction, the “equivalent luminance contrast” required for such cancellation is reduced when colour vision is abnormal. We used a consumer-grade infrared eye-tracker to measure eye movements made in response to coloured patterns drifting at different speeds. An automated analysis of these movements estimated individuals’ red-green equiluminant point and their equivalent luminance contrast. We tested 34 participants: 23 colour vision normal controls, 9 deuteranomalous and 2 protanomalous individuals. We obtained reliable estimates of strength of directed eye movements (i.e. combined optokinetic and voluntary tracking) for stimuli moving at 16 deg/s and could use these data to classify participants’ colour vision status with a sensitivity rate of 90.9% and a specificity rate of 91.3%. We conclude that an objective test of functional colour vision combining a motion-nulling technique with an automated analysis of eye movements can diagnose and assess the severity of protanopia and deuteranopia. The test places minimal demands on patients (who simply view a series of moving patterns for less than 90 s), requires modest operator expertise, and can be run on affordable hardware.