Visual illusions and neurobiology.
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Biomedical subjects
Publications and source records attributed to D M Eagleman.
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When a flash is aligned with a moving object, subjects perceive the flash to lag behind the moving object. Two different models have been proposed to explain this "flash-lag" effect. In the motion extrapolation model, the visual system extrapolates the location of the moving object to counteract neural propagation delays, whereas in the latency difference model, it is hypothesized that moving objects are processed and perceived more quickly than flashed objects. However, recent psychophysical experiments suggest that neither of these interpretations is feasible (Eagleman & Sejnowski, 2000a, 2000b, 2000c), hypothesizing instead that the visual system uses data from the future of an event before committing to an interpretation. We formalize this idea in terms of the statistical framework of optimal smoothing and show that a model based on smoothing accounts for the shape of psychometric curves from a flash-lag experiment involving random reversals of motion direction. The smoothing model demonstrates how the visual system may enhance perceptual accuracy by relying not only on data from the past but also on data collected from the immediate future of an event.
In the flash-lag illusion, a flash and a moving object in the same location appear to be offset. A series of psychophysical experiments yields data inconsistent with two previously proposed explanations: motion extrapolation (a predictive model) and latency difference (an online model). We propose an alternative in which visual awareness is neither predictive nor online but is postdictive, so that the percept attributed to the time of the flash is a function of events that happen in the approximately 80 milliseconds after the flash. The results here show how interpolation of the past is the only framework of the three models that provides a unified explanation for the flash-lag phenomenon.
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Extracellular calcium is critical for many neural functions, including neurotransmission, cell adhesion, and neural plasticity. Experiments have shown that normal neural activity is associated with changes in extracellular calcium, which has motivated recent computational work that employs such fluctuations in an information-bearing role. This possibility suggests that a new style of computing is taking place in the mammalian brain in addition to current 'circuit' models that use only neurons and connections. Previous computational models of rapid external calcium changes used only rough approximations of calcium channel dynamics to compute the expected calcium decrements in the extracellular space. Using realistic calcium channel models, experimentally measured back-propagating action potentials, and a model of the extracellular space, we computed the fluctuations in external calcium that accrue during neural activity. In this realistic setting, we showed that rapid, significant changes in local external calcium can occur when dendrites are invaded by back-propagating spikes, even in the presence of an extracellular calcium buffer. We further showed how different geometric arrangements of calcium channels or dendrites prolong or amplify these fluctuations. Finally, we computed the influence of experimentally measured synaptic input on peridendritic calcium fluctuations. Remarkably, appropriately timed synaptic input can amplify significantly the decrement in external calcium. The model shows that the extracellular space and the calcium channels that access it provide a medium that naturally integrates coincident spike activity from different dendrites that intersect the same tissue volume.