Abstract
Motion-induced blindness (MIB) occurs when a dot embedded in a motion field subjectively vanishes. Here we report the first psychophysical data concerning effects of microsaccade/eyeblink rate upon perceptual switches during MIB. We find that the rate of microsaccades/eyeblink rises before and after perceptual transitions from not seeing to seeing the dot, and decreases before perceptual transitions from seeing it to not seeing it. In addition, event-related fMRI data reveal that, when a dot subjectively reappears during MIB, the blood oxygen-level dependent (BOLD) signal increases in V1v and V2v and decreases in contralateral hMT+. These BOLD signal changes observed upon perceptual state changes in MIB could be driven by the change of perceptual states and/or a confounding factor, such as the microsaccade/eyeblink rate.
Highlights
When high-contrast stationary stimuli, such as dots, are embedded within a global moving pattern, such as a rotating field of crosses, the dots seem to disappear and reappear alternately, they are constantly present in the stimulus [1]
In general, early visual areas have a stronger blood oxygen-level dependent (BOLD) activation after a perceptual switch (Figure 5) such that signal intensity rises after perceptual transitions from ‘no see’ to ‘see’ for the case where the dot was present in the corresponding contralateral quadrant
An increase in microsaccade rate before target reappearance from perceptual fading was recently reported [14]. This finding confirms that microsaccades or blinks likely break the bottom-up local sensory adaptation to edge information that is presumably necessary for perceptual fading to occur
Summary
When high-contrast stationary stimuli, such as dots, are embedded within a global moving pattern, such as a rotating field of crosses, the dots seem to disappear and reappear alternately, they are constantly present in the stimulus [1]. Perceptual filling-in is known as ‘perceptual fading’ or ‘The Troxler effect’ [4], which occurs when an object, though present in the world and continually casting light upon the retina, vanishes from visual consciousness to be replaced by its surrounding background. This phenomenon is commonly thought to arise because of bottom-up local sensory adaptation to edge information [5] and is presumed to occur early in the visual pathway, such as in the lateral geniculate nucleus of the thalamus (LGN) or even retinal ganglion cells [6,7,8]. Retinal adaptation could lead to a weakened edge signal sent from retinal ganglion cells, followed by a cortical filling-in process [9,10]
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