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Stephen L Macknik

Publications and source records attributed to Stephen L Macknik.

7 recordsLinked to original sources

Microsaccades counteract visual fading during 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.

Adult↗

Visual masking approaches to visual awareness.

In visual masking, visible targets are rendered invisible by modifying the context in which they are presented, but not by modifying the targets themselves. Here I summarize a decade of experimentation using visual masking illusions in which my colleagues and I have begun to establish the minimal set of conditions necessary to maintain the awareness of the visibility of simple unattended stimuli. We have established that spatiotemporal edges must be present for targets to be visible. These spatiotemporal edges must be encoded by transient bursts of spikes in the early visual system. If these bursts are inhibited, visibility fails. Target-correlated activity must rise within the visual hierarchy at least to the level of V3, and be processed within the occipital lobe, to achieve visibility. The specific circuits that maintain visibility are not yet known, but we have deduced that lateral inhibition plays a critical role in sculpting our perception of visibility, both by causing interactions between stimuli positioned across space, and also by shaping the responses to stimuli across time. Further, the studies have served to narrow the number of possible theories to explain visibility and visual masking. Finally, we have discovered that lateral inhibition builds iteratively in strength throughout the visual hierarchy, for both monoptic and dichoptic stimuli. Since binocular information is not integrated until inputs from the two eyes reach the primary visual cortex, it follows that the early visual areas contain differential levels of monoptic and dichoptic lateral inhibitions. We exploited this fact to discover that excitatory integration of binocular inputs occurs at an earlier level than interocular suppression. These findings are potentially fundamental to our understanding of all forms of binocular vision and to determining the role of binocular rivalry in visual awareness.

Animals↗

Visibility, visual awareness, and visual masking of simple unattended targets are confined to areas in the occipital cortex beyond human V1/V2.

In visual masking, visible targets are rendered invisible by modifying the context in which they are presented, but not by modifying the targets themselves. Here, we localize the neuronal correlates of visual awareness in the human brain by using visual masking illusions. We compare monoptic visual masking activation, which we find within all retinotopic visual areas, with dichoptic masking activation, which we find only in those retinotopic areas downstream of V2. Because monoptic and dichoptic masking are equivalent in magnitude perceptually, the present results establish a lower bound for maintenance of visual awareness of simple unattended targets. Moreover, we find that awareness-correlated circuits for simple targets are restricted to the occipital lobe. This finding provides evidence of an upper boundary in the visual hierarchy for visual awareness of simple unattended targets, thus constraining the location of circuits that maintain the visibility of simple targets to occipital areas beyond V1/V2.

Adolescent↗

Novel visual illusions related to Vasarely's 'nested squares' show that corner salience varies with corner angle.

Vasarely's 'nested-squares' illusion shows that 90 degrees corners can be more salient perceptually than straight edges. On the basis of this illusion we have developed a novel visual illusion, the 'Alternating Brightness Star', which shows that sharp corners are more salient than shallow corners (an effect we call 'corner angle salience variation') and that the same corner can be perceived as either bright or dark depending on the polarity of the angle (ie whether concave or convex: 'corner angle brightness reversal'). Here we quantify the perception of corner angle salience variation and corner angle brightness reversal effects in twelve naive human subjects, in a two-alternative forced-choice brightness discrimination task. The results show that sharp corners generate stronger percepts than shallow corners, and that corner gradients appear bright or dark depending on whether the corner is concave or convex. Basic computational models of center surround receptive fields predict the results to some degree, but not fully.

Adult↗

The function of bursts of spikes during visual fixation in the awake primate lateral geniculate nucleus and primary visual cortex.

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, microsaccade-generated 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.

Animals↗

Dichoptic visual masking reveals that early binocular neurons exhibit weak interocular suppression: implications for binocular vision and visual awareness.

Visual masking effects are illusions in which a target is rendered invisible by a mask, which can either overlap or not overlap the target spatially and/or temporally. These illusions provide a powerful tool to study visibility and consciousness, object grouping, brightness perception, and much more. As such, the physiological mechanisms underlying the perception of masking are critically important to our understanding of visibility. Several models that require cortical circuits have been proposed previously to explain the mysterious spatial and timing effects associated with visual masking. Here we describe single-unit physiological experiments from the awake monkey that show that visual masking occurs in at least two separate and independent circuits, one that is binocular and one that is monocular (possibly even subcortical), without feedback from higher-level visual brain areas. These and other results together fail to support models of masking that require circuits found only in the cortex, but support our proposed model that suggests that simple ubiquitous lateral inhibition may itself be the fundamental mechanism that explains visual masking across multiple levels in the brain. We also show that area V1 neurons are dichoptic in terms of excitation, but monoptic in terms of inhibition. That is, responses within area V1 binocular neurons reveal that excitation to monocular targets is inhibited strongly only by masks presented to the same eye, and not by masks presented to the opposite eye. These results lead us to redefine the model for the first stage of binocular processing in the visual system, and may be crucial to interpreting the effects of other similar binocular and dichoptic stimulation paradigms, such as the binocular rivalry family of illusions.

Action Potentials↗