August 2016
Volume 16, Issue 12
Open Access
Vision Sciences Society Annual Meeting Abstract  |   September 2016
Sensory eye dominance due to interocular imbalances of inhibition and integration
Author Affiliations
  • Chao Han
    College of Optometry, The Ohio State University
  • Teng-Leng Ooi
    College of Optometry, The Ohio State University
  • Zijiang He
    Department of Psychological and Brain Sciences, University of Louisville
Journal of Vision September 2016, Vol.16, 828. doi:10.1167/16.12.828
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      Chao Han, Teng-Leng Ooi, Zijiang He; Sensory eye dominance due to interocular imbalances of inhibition and integration. Journal of Vision 2016;16(12):828. doi: 10.1167/16.12.828.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Sensory eye dominance (SED) refers to an unbalanced interocular contribution to binocular interaction. Generally, SED is larger in amblyopes than non-amblyopes, and perceptual learning protocols that reduce SED can improve stereopsis (Xu et al, 2010; Ooi et al, 2013). However, since binocular interaction includes both interocular integration and interocular inhibitory processes, it is important to investigate the interocular imbalance within each process (SED-integration and SED-inhibition). Experimentally, SED-integration can be measured by using dichoptic stimuli with similar image features, such as horizontal gratings with relative phase shifts (e.g., Ding & Sperling, 2006). In contrast, SED-inhibition can be measured with orthogonal gratings that induce binocular rivalry (e.g., Ooi & He 2001). An outstanding question is whether SED-integration and SED-inhibition are related as no study has yet measured both forms of SED on the same observers. To answer this, we measured SED-integration and SED-inhibition of observers with clinically normal vision (at least 20/20 visual acuity and 40" stereopsis). We also measured their stereo thresholds for detecting crossed and uncrossed disparity of random dot stereograms. And to explore whether SED has a possible contribution from the monocular pathways, we measured monocular contrast sensitivity. We found a high probability that the strong eye revealed in SED-integration was also the strong eye in SED-inhibition measurement even if the extents of SED were different. Observers with larger SED of either form tended to have higher stereo threshold for both crossed and uncrossed disparity. Observers with larger SED of either form could also have an interocular difference in contrast sensitivity, which nevertheless could not fully account for the SED. Taken together, our results suggest that while SED-integration and SED-inhibition reflect interocular imbalances, respectively in the excitatory and inhibitory processes, we cannot rule out the possibility that both forms of interocular imbalances are triggered by a common cause.

Meeting abstract presented at VSS 2016

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