Contributions of Parvocelular and Magnocellular Pathways to Metacontrast and Target Recovery

Abstract

The visibility of a target stimulus (T) can be reduced by an aftercoming and spatially non-overlapping mask stimulus (M1), a phenomenon known as metacontrast masking. Interestingly, the visibility of the masked target can be recovered when a secondary mask (M2) is added to the T-M1 sequence. We analyzed a computational model of retino-cortical dynamics (RECOD) and derived the prediction that contrast dependence of metacontrast and target recovery should parallel the contrast dependence of afferent magnocellular and parvocellular pathways, respectively. In a psychophysical experiment, we tested this prediction by varying systematically M2's contrast. At the optimal T-M2 stimulus onset asynchrony (SOA), target recovery effect increased with M2's contrast without saturating, but at the optimal T-M2 metacontrast SOA, M1's visibility saturated very rapidly. Quantitative comparisons of psychophysical results with model simulations provide strong support for our prediction. We conclude that metacontrast masking is driven by signals originating from the magnocellular pathway and target recovery in metacontrast is driven by signals originating from the parvocellular pathway. These findings provide a link between the dynamics of the visual system and the architecture of the underlying neural processes