With every rapid gaze shift (saccade), our eyes experience a different view of the world. Stable perception of visual space requires that points in the new image are associated with corresponding points in the previous image. The brain may use an extraretinal eye position signal to compensate for gaze changes, or, alternatively, exploit the image contents to determine associated locations. Support for a uniform extraretinal signal comes from findings that the apparent position of objects briefly flashed around the time of a saccade is often shifted in the direction of the saccade. This view is challenged, however, by observations that the magnitude and direction of the displacement varies across the visual field. Led by the observation that non-uniform displacements typically occurred in studies conducted in slightly illuminated rooms, here we determine the dependence of perisaccadic mislocalization on the availability of visual spatial references at various times around a saccade. We find that presaccadic compression occurs only if visual references are available immediately after, rather than before or during, the saccade. Our findings indicate that the visual processes of transsaccadic spatial localization use mainly postsaccadic visual information.

Objects flashed briefly around the time of a saccadic eye movement are grossly mislocalized by human subjects, so they appear to be compressed toward the endpoint of the saccade. In this study, we investigate spatial localization during saccadic adaptation to examine whether the focus of compression tends toward the intended saccadic target or at the endpoint of the actual (adapted) movement. We report two major results. First, that peri-saccadic focus of the compression did not occur at the site of the initial saccadic target, but tended toward the actual landing site of the saccade. Second, and more surprisingly, we observed a large long-term perceptual distortion of space, lasting for hundreds of milliseconds. This distortion did not occur over the whole visual field but was limited to a local region of visual space around the saccade target, suggesting that saccadic adaptation induces a visuo-topic remapping of space. The results imply that the mechanisms controlling saccadic adaptation also affect perception of space and point to a strong perceptual plasticity coordinated with the well-documented plasticity of the motor system.

The perceptual localization of objects flashed at the time of a saccade often shows large spatial distortions. These perisaccadic mislocalizations exhibit different spatial patterns depending on the experimental condition. In darkness, when only extraretinal information is available, mislocalization is spatially uniform. In light and when visual references are available, mislocalization is directed toward the saccade target, resembling a compression of visual space. These patterns are derived from measurements of the absolute perceived position of the flashed object in egocentric space. Here, we report that also the perceived location of the saccade target is altered when an object is flashed perisaccadically. The mislocalization of the target depends on the presentation time of the flashed object and is directed toward the position of the flash. The resulting compression of the relative distance between target and flash is similar in darkness and in light and can also be found during fixation. When the localization of the flashed object is described relative to the perceived location of the saccade target, spatial compression becomes similar in many experimental conditions. We therefore suggest that perisaccadic compression relies on an encoding of relative spatial locations of objects rather than on localizations in egocentric space.

The localization of peri-saccadically flashed objects shows two types of errors: first, a uniform shift in saccade direction, and second, a compression of visual space around the saccade target. Whereas the uniform shift occurs when the experiment is performed in complete darkness compression occurs when additional visual references are available. Thus peri-saccadic mislocalization contains motor and visual components. To distinguish between both factors we compared peri-saccadic localization errors during pro- and anti-saccades. In the case of anti-saccades, the visual cue that elicits the saccade and the actual eye movement are in opposite directions. We asked whether peri-saccadic compression can be observed with anti-saccades, and if so, whether the compression is directed toward the visual cue or follows the actual eye movement. In blocked trials, subjects performed saccades either toward a visual cue (pro-saccade) or to the mirrored position opposite to a visual cue (anti-saccade). Peri-saccadically, we flashed a thin vertical bar at one of four possible locations. Subjects had to indicate the perceived position of the bar with a mouse pointer about 500 ms after the saccade. Experiments were performed in complete darkness and with visual references. Peri-saccadic mislocalizations occurred during anti-saccades. The mislocalizations were very similar for pro- and anti-saccades in magnitude and direction. For both, pro- and anti-saccades, mislocalizations were directed toward the actual eye movement and not the visual cue.

. The neural mechanism that mediates perceptual filling-in of the blind spot is still under discussion. One hypothesis proposes that the cortical representation of the blind spot is activated only under conditions that elicit perceptual filling-in and requires congruent stimulation on both sides of the blind spot. Alternatively, the passive remapping hypothesis proposes that inputs from regions surrounding the blind spot infiltrate the representation of the blind spot in cortex. This theory predicts that independent stimuli presented to the left and right of the blind spot should lead to neighboring/overlapping activations in visual cortex when the blindspot eye is stimulated but separated activations when the fellow eye is stimulated. Using functional MRI, we directly tested the remapping hypothesis by presenting flickering checkerboard wedges to the left or right of the spatial location of the blind spot, either to the blind-spot eye or to the fellow eye. Irrespective of which eye was stimulated, we found separate activations corresponding to the left and right wedges. We identified the centroid of the activations on a cortical flat map and measured the distance between activations. Distance measures of the cortical gap across the blind spot were accurate and reliable (mean distance: 6 -8 mm across subjects, SD ϳ1 mm within subjects). Contrary to the predictions of the remapping hypothesis, cortical distances between activations to the two wedges were equally large for the blind-spot eye and fellow eye in areas V1 and V2/V3. Remapping therefore appears unlikely to account for perceptual filling-in at an early cortical level.

No abstract

No abstract

No abstract