Abstract
Recent studies that investigated perception around saccadic eye movements in illuminated rooms reported a mislocalization of briefly flashed stimuli towards the endpoint of the saccade (Ross et al., Nature, 1997; Lappe et al., Nature, 2000). Such a ‘compression’ of the visual space occurs even before the eye starts to move. While a number of other studies further investigated those phenomena, we are still missing a model based on the anatomy and neurophysiology in the brain. It has been speculated that the observations could originate from a ‘corollary discharge’ which shifts receptive fields in LIP (Duhamel et al., Science, 1992) prior to the eye movement. We suggest a model in which a reentry signal from movement related cells (e.g. FEF or SC) enters the pathway for perception (e.g. MT) and modulates the responses of the cells. We have earlier suggested in the context of attention that such reentry signals could implement a gain control (Hamker, J Vision, 2003). In order to quantitatively fit the model with our experimental data we computed the incoming stimulus population based on the receptive field size distribution and magnification in MT. Movement cells are fitted with an exponential function. Our model is strongly constrained by anatomy and single cell recordings so that only two free parameters are necessary. Our simulations show, that the population encoding the stimulus property gets shifted towards the endpoint of the planned saccade. Since the magnification results in asymmetric populations around the saccadic goal, the model predicts that the shift observed in the presence of visual landmarks can indeed be part of the (asymmetric) compression. Our model further predicts that ‘compression’ originates during perception, rather than as a consequence of the transformation of spatial reference frames. These findings argue that phenomena of spatial attention and saccadic compression can be unified by a spatial reentry theory.