Slow horizontal head and body rotation occurs in mice and rats when the visual field is rotated around them, and these optomotor movements can be produced reliably in a virtual-reality system. If one eye is closed, only motion in the temporal-to-nasal direction for the contralateral eye evokes the tracking response. When the maximal spatial frequency capable of driving the response ("acuity") was measured under monocular and binocular viewing conditions, the monocular acuity was identical to the binocular acuity measured with the same rotation direction. Thus, the visual capabilities of each eye can be measured under binocular conditions simply by changing the direction of rotation. Lesions of the visual cortex had no effect on the acuities measured with the virtual optokinetic system, whereas perceptual thresholds obtained previously with the Visual Water Task are. The optokinetic acuities were also consistently lower than acuity estimates from the Visual Water Task, but contrast sensitivities were the same or better. These data show that head-tracking in a virtual optokinetic drum is driven by subcortical, lower frequency, and contralateral pathways.
Developmentally regulated plasticity of vision has generally been associated with "sensitive" or "critical" periods in juvenile life, wherein visual deprivation leads to loss of visual function. Here we report an enabling form of visual plasticity that commences in infant rats from eye opening, in which daily threshold testing of optokinetic tracking, amid otherwise normal visual experience, stimulates enduring, visual cortex-dependent enhancement (Ͼ60%) of the spatial frequency threshold for tracking. The perceptual ability to use spatial frequency in discriminating between moving visual stimuli is also improved by the testing experience. The capacity for inducing enhancement is transitory and effectively limited to infancy; however, enhanced responses are not consolidated and maintained unless in-kind testing experience continues uninterrupted into juvenile life. The data show that selective visual experience from infancy can alone enable visual function. They also indicate that plasticity associated with visual deprivation may not be the only cause of developmental visual dysfunction, because we found that experientially inducing enhancement in late infancy, without subsequent reinforcement of the experience in early juvenile life, can lead to enduring loss of function.
The unexpected lack of correlation of OKT testing with photoreceptor degeneration in the Tg rats emphasizes the need in behavioral therapeutic studies for careful analysis of visual thresholds of experimental animals prior to therapeutic intervention.
The ability of immunoprivileged Schwann cell transplants to preserve vision in RCS rats indicates that transplantation of syngeneic Schwann cells holds promise as a preventive treatment for retinal degenerative disease.
A large heterogeneous group of EPs can perform POCUS with high specificity but only intermediate sensitivity for RD. A negative POCUS scan in the ED performed by a heterogeneous group of providers after a one-hour POCUS didactic is not sufficiently sensitive to rule out RD in a patient with new onset flashes or floaters. This article is protected by copyright. All rights reserved.
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