Simultaneous adaptation to non-collinear retinal motion and smooth pursuit eye movement

Abstract

Simultaneously adapting to retinal motion and non-collinear pursuit eye movement produces a motion aftereffect (MAE) that moves in a different direction to either of the individual adapting motions. Mack, Hill and Kahn (1989, Perception, 18, 649-655) suggested that the MAE was determined by the perceived motion experienced during adaptation. We tested the perceived-motion hypothesis by having observers report perceived direction during simultaneous adaptation. For both central and peripheral retinal motion adaptation, perceived direction did not predict the direction of subsequent MAE. To explain the findings we propose that the MAE is based on the vector sum of two components, one corresponding to a retinal MAE opposite to the adapting retinal motion and the other corresponding to an extra-retina MAE opposite to the eye movement. A vector model of this component hypothesis showed that the MAE directions reported in our experiments were the result of an extra-retinal component that was substantially larger in magnitude than the retinal component when the adapting retinal motion was positioned centrally. However, when retinal adaptation was peripheral, the model suggested the magnitude of the components should be about the same. These predictions were tested in a final experiment that used a magnitude estimation technique. Contrary to the predictions, the results showed no interaction between type of adaptation (retinal or pursuit) and the location of adapting retinal motion. Possible reasons for the failure of component hypothesis to fully explain the data are discussed.

Motion adaptation reveals that the motion vector is represented in multiple coordinate frames

“…Uncontrolled retinal motion due to the lack of eye tracking, the use of static test stimuli, the very slow pursuit speed, or the performance of the experiments in full light might all explain these contradicting results. Contrary to Anstis and Gregory's results, Davies and Freeman (2011) did find a MAE in a configuration resembling our Screen condition. Like them, Mack et al (1987) could not replicate Anstis and Gregory's results and showed that the MAE size depended on the induced motion of visual edges that appear to move due to SPEM.…”

“…A different perspective from ours was taken by studies asking whether the MAE could result from the efference copy of the oculomotor signal on its own (Chaudhuri, 1990a(Chaudhuri, , 1991Davies & Freeman, 2011;Freeman, 2007;Freeman & Sumnall, 2005;Freeman et al, 2003). All these studies have suggested that the degree of MAE generated during smooth pursuit is linked to the repetitive SPEM (pursuit followed by a saccade back to the starting location, followed by pursuit, etc.).…”

“…The MAE could possibly result from a pursuit oculomotor signal per se, without any important role of the visual random-dot stimulus in the background (Chaudhuri, 1990a(Chaudhuri, , 1991Davies & Freeman, 2011;Freeman, 2007;Freeman & Sumnall, 2005). To rule this out, we conducted another control experiment, the Pursuit Only (PO) adaptation condition, which was performed by eight of the original subjects.…”

“…The MAE was determined by the relative motion of the central grating with respect to the flanking gratings. Other extraretinal oculomotor elements that can be incorporated at different stages in the motion processing pathway can also induce a MAE (Chaudhuri, 1990a(Chaudhuri, , 1991Davies & Freeman, 2011;Freeman, 2007;Freeman & Sumnall, 2005;Freeman, Sumnall, & Snowden, 2003;Haarmeier, Bunjes, Lindner, Berret, & Thier, 2001). The integration of such nonvisual signals with retinal motion information may result in the representation of veridical motion, such that it allows discriminating between movement caused by gaze shifts (e.g., smooth pursuit) and movement in the real world.…”

“…The perceptual registration of this efferent signal produces the MAE. Others demonstrated that an efference copy of the eye movements can induce a MAE which can be combined with the retinally induced MAE at subcortical or cortical levels (Davies & Freeman, 2011;Freeman, 2007;Freeman & Sumnall, 2005;Freeman et al, 2003;Haarmeier et al, 2001).…”