Background: The aim of the study was to demonstrate the influence of virtual reality (VR) exposure on postural stability and determine the mechanism of this influence. Methods: Twenty-six male participants aged 21-23 years were included, who underwent postural stability assessment twice before and after a few minute of single VR exposure. The VR projection was a computer-generated simulation of the surrounding scenery. Postural stability was assessed using the Sensory Organization Test (SOT), using Computerized Dynamic Posturography (CDP). Results: The findings indicated that VR exposure affects the visual and vestibular systems. Significant differences (p < 0.05) in results before and after VR exposure were observed in tests on an unstable surface. It was confirmed that VR exposure has a positive influence on postural stability, attributed to an increase in the sensory weight of the vestibular system. Partial evidence suggested that the reduction in vestibulo-ocular reflex (VOR) reinforcement may result in an adaptive shift to the optokinetic reflex (OKR). Conclusions: By modifying the process of environmental perception through artificial sensory simulation, the influence of VR on postural stability has been demonstrated. The validity of this type of research is determined by the effectiveness of VR techniques in the field of vestibular rehabilitation.

One-sided vestibular disorders are common in clinical practice; however, their models have not been fully established. We investigated the effect of unilateral or bilateral deficits in the vestibular organs on the vestibulo-ocular reflex (VOR) and optokinetic reflex (OKR) of zebrafish using in-house equipment. For physical dislodgement of the otoliths in the utricles of zebrafish larvae, one or both utricles were separated from the surrounding tissue using glass capillaries. The video data from VOR and OKR tests with the larvae was collected and processed using digital signal processing techniques such as fast Fourier transform and low-pass filters. The results showed that unilateral and bilateral damage to the vestibular system significantly reduced VOR and OKR. In contrast, no significant difference was observed between unilateral and bilateral damage. This study confirmed that VOR and OKR were significantly reduced in zebrafish with unilateral and bilateral vestibular damage. Follow-up studies on unilateral vestibular disorders can be conducted using this tool.

To generate a coherent visual percept, information from both eyes must be appropriately transmitted into the brain, where binocular integration forms the substrate for visuomotor behaviors. To establish the anatomical substrate for binocular integration, the presence of bilateral eyes and interaction of both optic nerves during retinotectal development play a key role. However, the extent to which embryonic monocularly derived visual circuits can convey visuomotor behaviors is unknown. In this study, we assessed the retinotectal anatomy and visuomotor performance of embryonically generated one-eyed tadpoles. In one-eyed animals, the axons of retinal ganglion cells from the singular remaining eye exhibited striking irregularities in their central projections in the brain, generating a noncanonical ipsilateral retinotectal projection. This data is indicative of impaired pathfinding abilities. We further show that these novel projections are correlated with an impairment of behavioral compensation for the loss of one eye.

Animals constantly redirect their gaze away or towards relevant targets and, besides these goal-oriented responses, stabilizing movements clamp the visual scene avoiding image blurring. The vestibulo-ocular (VOR) and the optokinetic reflexes are the main contributors to gaze stabilization, whereas the optic tectum integrates multisensory information and generates orienting/evasive gaze movements in all vertebrates. Lampreys show a unique stepwise development of the visual system whose understanding provides important insights into the evolution and development of vertebrate vision. Although the developmental emergence of the visual components, and the retinofugal pathways have been described, the functional development of the visual system and the development of the downstream pathways controlling gaze are still unknown. Here, we show that VOR followed by light-evoked eye movements are the first to appear already in larvae, despite their burrowed lifestyle. However, the circuits controlling goal-oriented responses emerge later, in larvae in non-parasitic lampreys but during late metamorphosis in parasitic lampreys. The appearance of stabilizing responses earlier than goal-oriented in the lamprey development shows a stepwise transition from simpler to more complex visual systems, offering a unique opportunity to isolate the functioning of their underlying circuits.

The restructuring of the gaze stabilization system in Pelobates fuscus was investigated by quantitative analysis of the optomotor response using video imaging. Gaze stabilization is an important component in the system of neural mechanisms of visual depth perception. It was shown that the optomotor response in aquatic tadpoles of P. fuscus is similar to that of fish (movement of the animal in the direction of the visual background movement and eye nystagmus consisting of a fast and a slow phase). During metamorphosis (transition from the aquatic to the terrestrial lifestyle), froglets of P. fuscus responded to the movement of the visual background by eyes and head movements. One year after metamorphosis, P. fuscus responded to movement of the visual background as adult Anura: only by head movements (a slow and a fast phase), while eye movements were absent. Possible causes of the loss of active eye movements by Anura amphibians in the process of evolution are discussed.

BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.

Spinocerebellar Ataxia Type 6 (SCA6) is a mid-life onset neurodegenerative disease characterized by progressive ataxia, dysarthria, and eye movement impairment. This autosomal dominant disease is caused by the expansion of a CAG repeat tract in the CACNA1A gene that encodes the α1A subunit of the P/Q type voltage-gated Ca2+ channel. Mouse models of SCA6 demonstrate impaired locomotive function and reduced firing precision of cerebellar Purkinje in the anterior vermis. Here, to further assess deficits in other cerebellar-dependent behaviors, we characterized the oculomotor phenotype of a knock-in mouse model with hyper-expanded polyQ repeats (SCA684Q). We found a reduction in the efficacy of the vestibulo-ocular reflex (VOR) and optokinetic reflex (OKR) in SCA6 mutant mice, without a change in phase, compared to their litter-matched controls. Additionally, VOR motor learning was significantly impaired in SCA684Q mice. Given that the floccular lobe of the cerebellum plays a vital role in the generation of OKR and VOR calibration and motor learning, we investigated the firing behavior and morphology of floccular cerebellar Purkinje cells. Overall, we found a reduction in the firing precision of floccular lobe Purkinje cells but no morphological difference between SCA684Q and wild-type mice. Taken together, our findings establish that gaze stabilization and motor learning are impaired in SCA684Q mice and suggest that altered cerebellar output contributes to these deficits.

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.

The angular vestibulo-ocular reflex (aVOR) stabilizes retinal images by counter-rotating the eyes during head rotations. Perfect compensatory movements would thus rotate the eyes exactly opposite to the head, that is, eyes vs. head would exhibit a unity gain. However, in many species, but also in elderly humans or patients with a history of vestibular damage, the aVOR is far from compensatory with gains that are in part considerably lower than unity. The reason for this apparent suboptimality is unknown. Here, we propose that low VOR gain values reflect an optimal adaptation to sensory and motor signal variability. According to this hypothesis, gaze stabilization mechanisms that aim at minimizing the overall retinal image slip must consider the effects of (1) sensory and motor noise and (2) dynamic constraints of peripheral and central nervous processing. We demonstrate that a computational model for optimizing retinal image slip in the presence of such constraints of signal processing in fact predicts gain values smaller than unity. We further show specifically for tadpoles of the clawed toad, Xenopus laevis with particularly low gain values that previously reported VOR gains quantitatively correspond to the observed variability of eye movements and thus constitute an optimal adaptation mechanism. We thus hypothesize that lower VOR gain values in elderly human subjects or recovered patients with a history of vestibular damage may be the sign of an optimization given higher noise levels rather than a direct consequence of the damage, such as an inability of executing fast compensatory eye movements.

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.