Microsaccades are known to occur during prolonged visual fixation, but it is a matter of controversy whether they also happen during free-viewing. Here we set out to determine: 1) whether microsaccades occur during free visual exploration and visual search, 2) whether microsaccade dynamics vary as a function of visual stimulation and viewing task, and 3) whether saccades and microsaccades share characteristics that might argue in favor of a common saccade-microsaccade oculomotor generator. Human subjects viewed naturalistic stimuli while performing various viewing tasks, including visual exploration, visual search, and prolonged visual fixation. Their eye movements were simultaneously recorded with high precision. Our results show that microsaccades are produced during the fixation periods that occur during visual exploration and visual search. Microsaccade dynamics during free-viewing moreover varied as a function of visual stimulation and viewing task, with increasingly demanding tasks resulting in increased microsaccade production. Moreover, saccades and microsaccades had comparable spatiotemporal characteristics, including the presence of equivalent refractory periods between all pair-wise combinations of saccades and microsaccades. Thus our results indicate a microsaccade-saccade continuum and support the hypothesis of a common oculomotor generator for saccades and microsaccades.
A brief visual target stimulus may be rendered invisible if it is immediately preceded or followed by another stimulus. This class of illusions, known as visual masking, may allow insights into the neural mechanisms that underlie visual perception. We have therefore explored the temporal characteristics of masking illusions in humans, and compared them with corresponding neuronal responses in the primary visual cortex of awake and anesthetized monkeys. Stimulus parameters that in humans produce forward masking (in which the mask precedes the target) suppress the transient on-response to the target in monkey visual cortex. Those that produce backward masking (in which the mask comes after the target) inhibit the transient after-discharge, the excitatory response that occurs just after the disappearance of the target. These results suggest that, for targets that can be masked (those of short duration), the transient neuronal responses associated with onset and turning off of the target may be important in its visibility.
When we attempt to fix our gaze, our eyes nevertheless produce so-called 'fixational eye movements', which include microsaccades, drift and tremor. Fixational eye movements thwart neural adaptation to unchanging stimuli and thus prevent and reverse perceptual fading during fixation. Over the past 10 years, microsaccade research has become one of the most active fields in visual, oculomotor and even cognitive neuroscience. The similarities and differences between microsaccades and saccades have been a most intriguing area of study, and the results of this research are leading us towards a unified theory of saccadic and microsaccadic function.
When viewing a stationary object, we unconsciously make small, involuntary eye movements or 'microsaccades'. If displacements of the retinal image are prevented, the image quickly fades from perception. To understand how microsaccades sustain perception, we studied their relationship to the firing of cells in primary visual cortex (V1). We tracked eye movements and recorded from V1 cells as macaque monkeys fixated. When an optimally oriented line was centered over a cell's receptive field, activity increased after microsaccades. Moreover, microsaccades were better correlated with bursts of spikes than with either single spikes or instantaneous firing rate. These findings may help explain maintenance of perception during normal visual fixation.
Our eyes move continually, even while we fixate our gaze on an object. If fixational eye movements are counteracted, our perception of stationary objects fades completely, due to neural adaptation. Some studies have suggested that fixational microsaccades refresh retinal images, thereby preventing adaptation and fading. However, other studies disagree, and so the role of microsaccades remains unclear. Here, we correlate visibility during fixation to the occurrence of microsaccades. We asked subjects to indicate when Troxler fading of a peripheral target occurs, while simultaneously recording their eye movements with high precision. We found that before a fading period, the probability, rate, and magnitude of microsaccades decreased. Before transitions toward visibility, the probability, rate, and magnitude of microsaccades increased. These results reveal a direct link between suppression of microsaccades and fading and suggest a causal relationship between microsaccade production and target visibility during fixation.
When images are stabilized on the retina, visual perception fades. During voluntary visual fixation, however, constantly occurring small eye movements, including microsaccades, prevent this fading. We previously showed that microsaccades generated bursty firing in the primary visual cortex (area V-1) in the presence of stationary stimuli. Here we examine the neural activity generated by microsaccades in the lateral geniculate nucleus (LGN), and in the area V-1 of the awake monkey, for various functionally relevant stimulus parameters. During visual fixation, microsaccades drove LGN neurons by moving their receptive fields across a stationary stimulus, offering a likely explanation of how microsaccades block fading during normal fixation. Bursts of spikes in the LGN and area V-1 were associated more closely than lone spikes with preceding microsaccades, suggesting that bursts are more reliable than are lone spikes as neural signals for visibility. In area V-1, microsaccadegenerated activity, and the number of spikes per burst, was maximal when the bar stimulus centered over a receptive field matched the cell's optimal orientation. This suggested burst size as a neural code for stimuli optimality (and not solely stimuli visibility). As expected, burst size did not vary with stimulus orientation in the LGN. To address the effectiveness of microsaccades in generating neural activity, we compared activity correlated with microsaccades to activity correlated with flashing bars. Onset responses to flashes were about 7 times larger than the responses to the same stimulus moved across the cells' receptive fields by microsaccades, perhaps because of the relative abruptness of flashes. When the visual world is stabilized on the retina, visual perception fades as a consequence of neural adaptation (1-4). But during normal vision we move our eyes involuntarily every few hundred milliseconds, even as we try to fixate our gaze on a small stimulus, preventing retinal stabilization and the associated fading of visibility. These fixational eye movements include ''microsaccades,'' small ballistic unidirectional eye movements that are generated at random intervals in all directions. Fixational eye movements, including microsaccades, have been correlated with stimulus visibility (5-8), and in a previous paper we showed that microsaccades increase the probability of firing in area V-1 cells by moving their receptive fields over stationary stimuli (9). Here we ask whether microsaccades might also induce an increase in neural activity at an earlier level, in the neurons of the lateral geniculate nucleus (LGN). We also ask how effective microsaccades are in generating neural activity by comparing them with previously characterized and well known visual stimuli, flashing bars. Finally, because transient neural firing (i.e., bursts of spikes) has been proposed as a neural code for the visibility of a stimulus (9-12), we also ask here whether bursts of spikes are used by the visual system to encode the salience of a stimulus. To answer thi...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.