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Haluk Ogmen, Bruno G. Breitmeyer, Steven Todd, Lynn Mardon; Double dissociation in target recovery: Effect of contrast. Journal of Vision 2004;4(8):74. doi: 10.1167/4.8.74.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose. A double dissociation occurs between the visibility and the masking effectiveness of a primary mask M1 when a secondary mask M2 is introduced into the target (T)-M1 sequence in metacontrast (Breitmeyer et al., 1981). According to the dual-channel RECOD model, the dissociation occurs because M1's visibility and masking effectiveness are based on distinct processes: sustained (parvocellular, P) and transient (magnocellular, M) channel activities, respectively. We tested this hypothesis by comparing contrast dependent changes in visibility and masking effectiveness in target recovery. Methods. The stimuli were a 0.75 deg disk (T), surrounded by two rings (M1 and M2), of thickness 0.5 deg and separation of 0.05 deg centered 1.5 deg above and 1 deg to the right of fixation. A match stimulus of the same dimensions as T or M1 was positioned symmetrically to the left of fixation. The T-M1 stimulus onset asynchrony (SOA) was set to 60 ms. M1–M2 SOA varied from −180 ms to 210 ms. M2's contrast varied to produce M1/M2 contrast ratios from 0.125 to 1.5. Results. For all M1/M2 contrast ratios, target recovery was maximal when M2 preceded M1 by 90 ms and absent at SOAs where M2 follows M1, and a double-dissociation existed between M1's visibility and ability to suppress T. More importantly, at the optimal M1–M2 SOA of −90 ms, target recovery effect increased with M2's contrast without saturating, but at the optimal M1–M2 metacontrast SOA of 60 ms, M1's visibility saturated very rapidly. Conclusion. Since the contrast dependencies of sustained P and transient M pathways parallel the contrast dependencies of M1's visibility and masking effectiveness, respectively, our results provide evidence that target-recovery is produced by sustained-channel activity whereas metacontrast masking is produced by transient-channel activity, a conclusion supported by the simulations of the RECOD model.
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