Environmental Enrichment Improves Vestibular Oculomotor Learning in Mice.

We assessed the behavioral effects of environmental enrichment on contrast sensitivity, reflexive eye movements and on oculomotor learning in mice that were housed in an enriched environment for a period of 3 weeks. Research has shown that a larger cage and a more complex environment have positive effects on the welfare of laboratory mice and other animals held in captivity. It has also been shown that environmental enrichment affects various behavior and neuroanatomical and molecular characteristics. We found a clear effect on oculomotor learning. Animals that were housed in an enriched environment learned significantly faster than controls that were housed under standard conditions. In line with existing literature, the enriched group also outperformed the controls in behavioral tests for explorative behavior. Meanwhile, both visual and reflexive oculomotor performance in response to visual and vestibular stimuli was unaffected. This points toward an underlying mechanism that is specific for motor learning, rather than overall motor performance.

Impairment of Long-Term Plasticity of Cerebellar Purkinje Cells Eliminates the Effect of Anodal Direct Current Stimulation on Vestibulo-Ocular Reflex Habituation.

Anodal direct current stimulation (DCS) of the cerebellum facilitates adaptation tasks, but the mechanism underlying this effect is poorly understood. We have evaluated whether the effects of DCS effects depend on plasticity of cerebellar Purkinje cells (PCs). Here, we have successfully developed a mouse model of cerebellar DCS, allowing us to present the first demonstration of cerebellar DCS driven behavioral changes in rodents. We have utilized a simple gain down vestibulo-ocular reflex (VOR) adaptation paradigm, that stabilizes a visual image on the retina during brief head movements, as behavioral tool. Our results provide evidence that anodal stimulation has an acute post-stimulation effect on baseline gain reduction of VOR (VOR gain in sham, anodal and cathodal groups are 0.75 ± 0.12, 0.68 ± 0.1, and 0.78 ± 0.05, respectively). Moreover, this anodal induced decrease in VOR gain is directly dependent on the PP2B medicated synaptic long-term potentiation (LTP) and intrinsic plasticity pathways of PCs.

Human gaze following response is affected by visual acuity.

The present study investigated how gaze following eye movements are affected by stimulus contrast and spatial frequency and by aberrations in central visual acuity due to refractive errors. We measured 30 healthy subjects with a range of visual acuities but without any refractive correction. Visual acuity was tested using a Landolt-C chart. Subjects were divided into three groups with low, intermediate, or good visual acuity. Gaze following responses (GFR) to moving Gabor patches were recorded by video-oculography. In each trial, the subjects were presented with a single Gabor patch with a specific spatial frequency and luminance contrast that moved sinusoidally in the horizontal plane. We observed that GFR gain decreased with increasing spatial frequency and decreasing contrast and was correlated with visual acuity. GFR gain was lower and decreased more for subjects with lower visual acuity; this was especially so for lower stimulus contrasts that are not tested in standard acuity tests. The largest differences between the groups were observed at spatial frequencies around 4 cpd and at contrasts up to 10%. Aberrations in central visual acuity due to refractive errors affect the GFR response depending on the contrast and spatial frequency of the moving stimulus. Measuring this effect may contribute to a better estimate of changes in visual function as a result of aging, disease, or treatments meant to improve vision.

Albino mice as an animal model for infantile nystagmus syndrome.

PURPOSE: Individuals with oculocutaneous albinism are predisposed to visual system abnormalities affecting the retina and retinofugal projections, which may lead to reduced visual acuity and Infantile Nystagmus Syndrome (INS). Due to absence of an established mammalian animal model, mechanisms underlying INS remain elusive. In this study, we screened wild-type mice of varying pigmentation for ocular motor abnormalities in order to identify a possible mouse model for INS. METHODS: Three albino mouse strains (CD1, BALB/c, DBA/1), and two normally pigmented strains (129S6, C57BL/6) were screened using infrared oculography. Varying visual stimuli (black or white background, stationary pattern, optokinetic, i.e., horizontally rotating pattern) were displayed to the full (fVF) or anterior visual field (aVF) of the restrained mouse. RESULTS: We found spontaneous nystagmus, specifically jerks and oscillations, in albino mice under all experimental conditions. Median eye velocity was between 0.8 and 3.4 deg/s, depending on the strain. In contrast, the eyes in pigmented mice were nearly stable with a median absolute eye velocity of below 0.4 deg/s. In albino mice, fVF optokinetic stimuli elicited an optokinetic response (OKR) in the correct direction, albeit with superimposed oscillations. However, aVF optokinetic stimuli evoked reversed OKR in these strains, a well known feature of INS. CONCLUSIONS: Based on our results, we endorse the investigated albino mouse strains as new animal models for INS.

Accelerated loss of hearing and vision in the DNA-repair deficient Ercc1(δ/-) mouse.

Age-related loss of hearing and vision are two very common disabling conditions, but the underlying mechanisms are still poorly understood. Damage by reactive oxygen species and other reactive cellular metabolites, which in turn may damage macromolecules such as DNA, has been implicated in both processes. To investigate whether DNA damage can contribute to age-related hearing and vision loss, we investigated hearing and vision in Ercc1(δ/-) mutant mice, which are deficient in DNA repair of helix-distorting DNA lesions and interstrand DNA crosslinks. Ercc1(δ/-) mice showed a progressive, accelerated increase of hearing level thresholds over time, most likely arising from deteriorating cochlear function. Ercc1(δ/-) mutants also displayed a progressive decrease in contrast sensitivity followed by thinning of the outer nuclear layer of the eyeball. The strong parallels with normal ageing suggest that unrepaired DNA damage can induce age-related decline of the auditory and visual system.