Change blindness is a phenomenon characterized by observers’ failure to notice seemingly obvious changes in their visual input. In most cases of change blindness in the literature, such unnoticed changes coincide with other visual transients. This research team studied slow change blindness, a related phenomenon that occurs even in the absence of visual disruptions when the change occurs sufficiently slowly, to determine whether it could be explained by conclusions from classic change blindness. Across three different slow change blindness experiments the team found that observers who consistently failed to notice the change had access to at least two memory representations of the changing display. One representation was precise but short lived: a detailed representation of the more recent stimulus states, but fragile. The other representation lasted longer but was fairly general: stable but too coarse to differentiate the various stages of the change. These findings suggest that, although multiple representations are formed, the failure to compare hypotheses might not explain slow change blindness; even if a comparison were made, the representations would be too sparse (longer term stores) or too fragile (short-lived stores) for such comparison to inform about the change.

Polar angle asymmetries (PAAs), the differences in perceptual experiences and performance across different regions of the visual field are present in various paradigms and tasks of visual perception. Currently, research in this area is sparse, particularly regarding the influence of PAAs during perceptual illusions, highlighting a gap in visual cognition studies. This work aims to fill this gap by measuring PAAs across the visual field during an illusion applied to test conscious vision widely.

Cells can compensate a disruptive change in one ion channel by compensatory changes in other channels. This work has simulated the adaptation of a multicellular aggregate of non-excitable cells to the electrophysiological perturbation produced by the external blocking of a cation channel. In the biophysical model employed, the researchers consider that this blocking provokes a cell depolarization that opens a voltage-gated calcium channel, thus allowing toxic Ca2+ levels...