September 2017
Volume 17, Issue 10
Open Access
Vision Sciences Society Annual Meeting Abstract  |   August 2017
Microsaccades in blindsight monkeys
Author Affiliations
  • Masatoshi Yoshida
    Department of System Neuroscience, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
    School of Life Science, The Graduate University for Advanced Studies, Hayama 203-0193, Japan
  • Ziad Hafed
    Physiology of Active Vision Laboratory, Werner Reichardt Centre for Integrative Neuroscience, University of Tuebingen, Tuebingen, Germany
Journal of Vision August 2017, Vol.17, 896. doi:10.1167/17.10.896
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      Masatoshi Yoshida, Ziad Hafed; Microsaccades in blindsight monkeys. Journal of Vision 2017;17(10):896. doi: 10.1167/17.10.896.

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

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Abstract

Patients with damage to primary visual cortex (V1) demonstrate residual performance on laboratory visual tasks despite denial of conscious seeing (blindsight). Macaque monkeys with a unilateral V1 lesion have been used as an animal model for blindsight. After a period of recovery, these monkeys are able to localize visual stimuli in a forced-choice condition while failing to report awareness of identical stimuli in a yes-no detection task, which resembles human blindsight performance. Some residual attentional effects including saliency-guided eye movements and exogenous attention have also been demonstrated in blindsight monkeys. Here we examined whether microsaccades in blindsight monkeys are influenced by endogenous task instructions during Posner-style cueing. Before and after the unilateral removal of V1, two monkeys performed visually guided saccade tasks with a central informative cue. As a pre-cue, either an arrow or, in separate sessions, a color patch was superimposed for 100 ms on the fixation point. This was followed by a cue-target-onset asynchrony of 150-700 ms and then a saccade target at either the cued (80% of trials) or uncued (20% of trials) hemifield. Before the lesions, microsaccades were strongly affected by the cues, with an initial suppression in microsaccade frequency 50-150 ms after cue onset followed by rhythmic volleys of movements. Microsaccade directions were also modulated. After the lesions, there was a marked reduction in the number of microsaccades towards the affected hemifield during steady fixation (before cue onset). However, despite this bias, cue onset still caused modulations in microsaccades that were generally similar to those before the lesion. Consistent with this, the monkeys were also able to utilize the cues in the affected hemifield to direct their saccades to the cued target. These results help constrain models of microsaccade dynamics after peripheral and central cueing, and they highlight how V1 can contribute to such dynamics.

Meeting abstract presented at VSS 2017

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