Abstract
Brief monocular occlusion results in a transient change in ocular dominance, such that the previously patched eye makes a stronger contribution to the binocular percept after occlusion. The previously unpatched eye therefore makes a correspondingly weaker contribution to the binocular sum. To shed light on the mechanism underlying this change we investigate how the relationship between the perception of fusion, suppression, and diplopia changes after short-term monocular deprivation. Results show that fusible stimuli seen by the unpatched eye are actively suppressed as a result of patching and that this can be reversed by an interocular contrast imbalance. This suggests that dichoptic inhibition plays an important role in ocular dominance changes due to short-term occlusion, possibly by altering the contrast gain prior to binocular summation. This may help explain why this form of plasticity affects the perception of both fusible and rivalrous stimuli.
Highlights
Brief monocular occlusion results in a transient change in ocular dominance, such that the previously patched eye makes a stronger contribution to the binocular percept after occlusion
The first question is relevant to the previous approaches that have been used to quantify the effects of short-term plasticity due to monocular occlusion
We sought to answer whether the effects seen in these two approaches occur in the same underlying mechanism as would be the case if the patching effects targeted the contralateral inhibitory stage prior to binocular summation[14]
Summary
Brief monocular occlusion results in a transient change in ocular dominance, such that the previously patched eye makes a stronger contribution to the binocular percept after occlusion. Results show that fusible stimuli seen by the unpatched eye are actively suppressed as a result of patching and that this can be reversed by an interocular contrast imbalance This suggests that dichoptic inhibition plays an important role in ocular dominance changes due to short-term occlusion, possibly by altering the contrast gain prior to binocular summation. A unified explanation could be advanced in terms of the current two-stage model of binocular combination[14] where there are inhibitory inputs to the monocular contrast gain controls prior to excitatory combination (Fig. 1) These interactions occur before binocular combination they would still result in altered rates of rivalry for non-fusible stimuli as well as a change in dominance for fusible stimuli for example manifested as a shift of the position of the fused image in the direction of the dominant eye. Using a simple visual stimulus, blurred horizontal edge with different levels of blur/spatial scale (1, 2, 4, 8, 16, and 32 arcmin), vertical disparity (0, 1, 2, 3, 4, 5, 6, 7, and 8-times blur width), and interocular contrast offset (0, 6, and 12 dB) allowed them to evaluate the inter-relation between fusion, suppression, and diplopia in normal and abnormal visual www.nature.com/scientificreports/
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