Monocular perceptual learning has shown promising performance in restoring visual function in amblyopes beyond the critical period in the laboratory. However, the treatment outcome is variable and indeterminate in actual clinical and neuroscientific practice. We aimed to explore the efficacy of monocular perceptual learning in the clinical setting. By combining continuous monitoring of perceptual learning and clinical measurements, we evaluated the efficacy and characteristics of visual acuity and contrast sensitivity function improvement and further explored the individualized effect after perceptual learning. Amblyopes (average age:17 ± 7 years old) were trained in a monocular two-alternative forced choice identification task at the 50% contrast threshold of the amblyopic eye for 10-15 days. We found that monocular perceptual learning improves both visual acuity and contrast sensitivity function in amblyopia. The broader activation of spatial contrast sensitivity, with a significant improvement in lower spatial frequencies, contributed to improving visual acuity. Visual acuity changes in the early stage can predict the endpoint treatment outcomes. Our results confirm the efficacy of monocular perceptual learning and suggest potential predictors of training outcomes to assist in the future management of clinical intervention and vision neuroscience research in amblyopia beyond the critical period of visual plasticity.

During the visual critical period (CP), sensory experience refines the structure and function of visual circuits. The basis of this plasticity was long thought to be limited to cortical circuits, but recently described thalamic plasticity challenges this dogma and demonstrates greater complexity underlying visual plasticity. Yet how visual experience modulates thalamic neurons or how the thalamus modulates CP timing is incompletely understood. Using a larval zebrafish, thalamus-centric ocular dominance model, we show functional changes in the thalamus and a role of inhibitory signaling to establish CP timing using a combination of functional imaging, optogenetics, and pharmacology. Hemisphere-specific changes in genetically defined thalamic neurons correlate with changes in visuomotor behavior, establishing a role of thalamic plasticity in modulating motor performance. Our work demonstrates that visual plasticity is broadly conserved and that visual experience leads to neuron-level functional changes in the thalamus that require inhibitory signaling to establish critical period timing.

The decline of visual plasticity restricts the recovery of visual functions in adult amblyopia. Repetitive transcranial magnetic stimulation (rTMS) has been shown to be effective in treating adult amblyopia. However, the underlying mechanisms of rTMS on visual cortex plasticity remain unclear. In this study, we found that low-frequency rTMS reinstated the amplitude of visual evoked potentials, but did not influence the impaired depth perception of amblyopic rats. Furthermore, the expression of synaptic plasticity genes and the number of dendritic spines were significantly higher in amblyopic rats which received rTMS when compared with amblyopic rats which received sham stimulation, with reduced level of inhibition and perineuronal nets in visual cortex, as observed via molecular and histological investigations. The results provide further evidence that rTMS enhances functional recovery and visual plasticity in an adult amblyopic animal model.

Differences in morphology, ecology, and behavior through ontogeny can result in opposing selective pressures at different life stages. Most animals, however, transition through two or more distinct phenotypic phases, which is hypothesized to allow each life stage to adapt more freely to its ecological niche. How this applies to sensory systems, and in particular how sensory systems adapt across life stages at the molecular level, is not well understood. Here, we used whole-eye transcriptomes to investigate differences in gene expression between tadpole and juvenile southern leopard frogs (Lithobates sphenocephalus), which rely on vision in aquatic and terrestrial light environments, respectively. Because visual physiology changes with light levels, we also tested the effect of light and dark exposure.
We found 42% of genes were differentially expressed in the eyes of tadpoles versus juveniles and 5% for light/dark exposure. Analyses targeting a curated subset of visual genes revealed significant differential expression of genes that control aspects of visual function and development, including spectral sensitivity and lens composition. Finally, microspectrophotometry of photoreceptors confirmed shifts in spectral sensitivity predicted by the expression results, consistent with adaptation to distinct light environments.
Overall, we identified extensive expression-level differences in the eyes of tadpoles and juveniles related to observed morphological and physiological changes through metamorphosis and corresponding adaptive shifts to improve vision in the distinct aquatic and terrestrial light environments these frogs inhabit during their life cycle. More broadly, these results suggest that decoupling of gene expression can mediate the opposing selection pressures experienced by organisms with complex life cycles that inhabit different environmental conditions throughout ontogeny.

Recent studies show that the human adult visual system exhibits neural plasticity. For instance, short-term monocular deprivation shifts the eye dominance in favor of the deprived eye. This phenomenon is believed to occur in the primary visual cortex by reinstating neural plasticity. However, it is unknown whether the changes in eye dominance after monocularly depriving the visual input can also be induced by alternately depriving both eyes. In this study, we found no changes in binocular balance and interocular correlation sensitivity after a rapid (7 Hz), alternate and monocular deprivation for one hour in adults. Therefore, the effect of short-term monocular deprivation cannot seem to be emulated by alternately and rapidly depriving both eyes.Significance statementPrevious work has shown that short-term binocular function disruption, which its most extreme form is monocular deprivation, could induce neural plasticity in adult visual system. In this study, we found a balanced deprivation of binocular function could not induce a neuroplastic change in human adults. It appears that ocular dominance plasticity in human adults is unique in so far as it is only driven by an input imbalance not balanced deprivation of binocular function.

UNASSIGNED: To investigate whether short-term exposure to high temporal frequency full-field flicker has an impact on spatial visual acuity in individuals with varying degrees of myopia.
UNASSIGNED: Thirty subjects (evenly divided between control and experimental groups) underwent a 5-min exposure to full-field flicker. The flicker rate was lower than critical flicker frequency (CFF) for the experimental group (12.5 Hz) and significantly higher than CFF for the controls (60 Hz). Spatial contrast sensitivity function (CSF) was measured before and immediately after flicker exposure. We examined whether the post flicker CSF parameters were different from the pre-exposure CSF values in either of the subject groups. Additionally, we examined the relationship between the amount of CSF change from pre to post timepoints and the degree of subjects\' myopia. The CSF parameters included peak frequency, peak sensitivity, bandwidth, truncation, and area under log CSF (AULCSF).
UNASSIGNED: There was no significant difference of all five pre-exposure CSF parameters between the two groups at baseline (P = 0.333 ∼ 0.424). Experimental group subjects exhibited significant (P < 0.005) increases in peak sensitivity and AULCSF, when comparing post-exposure results to pre-exposure ones. Controls showed no such enhancements. Furthermore, the extent of these changes in the experimental group was correlated significantly with the participants\' refractive error (P = 0.005 and 0.018, respectively).
UNASSIGNED: Our data suggest that exposure to perceivable high-frequency flicker (but, not to supra-CFF frequencies) enhances important aspects of spatial contrast sensitivity, and these enhancements are correlated to the degree of myopia. This finding has implications for potential interventions for cases of modest myopia.

Schizophrenia is a severe mental illness with visual learning and memory deficits, and reduced long term potentiation (LTP) may underlie these impairments. Recent human fMRI and EEG studies have assessed visual plasticity that was induced with high frequency visual stimulation, which is thought to mimic an LTP-like phenomenon. This study investigated the differences in visual plasticity in participants with schizophrenia and healthy controls. An fMRI visual plasticity paradigm was implemented, and proton magnetic resonance spectroscopy data were acquired to determine whether baseline resting levels of glutamatergic and GABA metabolites were related to visual plasticity response. Adults with schizophrenia did not demonstrate visual plasticity after family-wise error correction; whereas, the healthy control group did. There was a significant regional difference in visual plasticity in the left visual cortical area V2 when assessing group differences, and baseline GABA levels were associated with this specific ROI in the SZ group only. Overall, this study suggests that visual plasticity is altered in schizophrenia and related to basal GABA levels.

Vertebrate rod and cone photoreceptors detect light via a specialized organelle called the outer segment. This structure is packed with light-sensitive molecules known as visual pigments that consist of a G-protein-coupled, seven-transmembrane protein known as opsin, and a chromophore prosthetic group, either 11-cis retinal (\'A1\') or 11-cis 3,4-didehydroretinal (\'A2\'). The enzyme cyp27c1 converts A1 into A2 in the retinal pigment epithelium. Replacing A1 with A2 in a visual pigment red-shifts its spectral sensitivity and broadens its bandwidth of absorption at the expense of decreased photosensitivity and increased thermal noise. The use of vitamin A2-based visual pigments is strongly associated with the occupation of aquatic habitats in which the ambient light is red-shifted. By modulating the A1/A2 ratio in the retina, an organism can dynamically tune the spectral sensitivity of the visual system to better match the predominant wavelengths of light in its environment. As many as a quarter of all vertebrate species utilize A2, at least during a part of their life cycle or under certain environmental conditions. A2 utilization therefore represents an important and widespread mechanism of sensory plasticity. This review provides an up-to-date account of the A1/A2 chromophore exchange system.

People with schizophrenia (SZ) exhibit visual processing abnormalities that affect their daily functioning and remediating these deficits might help to improve functioning. Transcranial direct current stimulation (tDCS) is a potential tool for perceptual enhancement for this purpose, though there are no reports of tDCS applied to visual cortex in SZ. In a within-subject, crossover design, we evaluated the effects of tDCS on visual processing in 27 SZ. All patients received anodal, cathodal, or sham stimulation over the central occipital region in 3 visits separated by 1 week. In each visit, a backward masking task and an electroencephalography measure of visual neuroplasticity were administered after tDCS. Neuroplasticity was assessed with visual evoked potentials before and after tetanizing visual high-frequency stimulation. Masking performance was significantly poorer in the anodal and cathodal conditions compared with sham. Both anodal and cathodal stimulation increased the amplitude of P1 but did not change the plasticity index. We found significant plasticity effects of tDCS for only one waveform for one stimulation condition (P2 for anodal tDCS) which did not survive correction for multiple comparisons. The reason for the lack of tDCS stimulation effects on plasticity may be because tDCS was not delivered simultaneously with the tetanizing visual stimulus. The present findings emphasize the need for more research on the relevant parameters for stimulation of visual processing regions in clinical populations.

Studies on binocular combination and rivalry show that short-term deprivation strengthens the contribution of the deprived eye in binocular vision. However, whether short-term monocular deprivation affects temporal processing per se is not clear. To address this issue, we conducted a study to investigate the effect of monocular deprivation on dichoptic temporal synchrony. We tested ten adults with normal vision and patched their dominant eye with an opaque patch for 2.5 h. A temporal synchrony paradigm was used to measure if temporal synchrony thresholds change as a result of monocular pattern deprivation. In this paradigm, we displayed two pairs of Gaussian blobs flickering at 1 Hz with either the same or different phased- temporal modulation. In Experiment 1, we obtained the thresholds for detecting temporal asynchrony under dichoptic viewing configurations. We compared the thresholds for temporal synchrony between before and after monocular deprivation and found no significant changes of the interocular synchrony. In Experiment 2, we measured the monocular thresholds for detecting temporal asynchrony. We also found no significant changes of the monocular synchrony of either the patched eye or the unpatched eye. Our findings suggest that short-term monocular deprivation induced-plasticity does not influence monocular or dichoptic temporal synchrony at low temporal frequency.