The motion after effect (MAE) is an illusion of movement resulting from prolonged perception of motion in the opposite direction (Collman, 2003) A good example of this would be staring for a while at a stationary point while a textured pattern drifts across the field of vision (e.g. a rock in the middle of a waterfall), then for a short while after the movement ceases one gazes at a stationary pattern (e.g. scenery next to the waterfall), apparent movement is seen in the opposite direction. (Mather, Verstraten & Antis, 1998)
Barlow and Hill (1963) suggested that MAE’s might result from the temporary discharges of cells responsive to motion in opposite directions. This suggests that in our visual system there are cells responsive for perceiving motion in specific directions (cells ‘tuned’ to motion in specific directions). The ratio model (or opponent process) first suggested by Sutherland (1961; as cited in Mather 1998) is much supported by the work of Barlow and Hill (1963). Direction selective cells tuned to opposite directions provide inputs to a comparator cell, one excitatory and one inhibitory. Perceived direction is said to depend on the difference between the outputs of the oppositely tuned detectors, as signalled by the comparators. Net excitation signifies upward motion. So motion is detected as thus, if the brain is shown something moving in a particular direction one cell will fire rapidly, there is more output given from this cells than its opponent cells and the brain interprets this as motion.
Motion after effects show interocular transfer (an effect is seen in the non-adapted eye) A motion after effect induced by inspecting an adapting motion with the left eye can be elicited by viewing a stationary test surface with the right eye. However interocular transfer does not indicate an origin central to the locus of binocular fusion because the adapted (left eye) might be sending up a retinal after effect signal which is combined somewhere in the brain with the signal of a stationary test field from the unadapted right eye. Barlow and Brindley (1963; as cited in Antis & Duncan, 1983) overcame this problem using the pressure blind technique. They found interocular transfer even when the adapted eye was pressure-blinded between looking at the adapting motion with one eye and examining for its after effect in the other. The MAE therefore did not reside in activity in the retinal ganglion cells.
Wohlegemuth (1911; as cited in Antis & Duncan, 1983) found MAE’s that lie in monoculary driven channels. He found that if one looks at a spiral with one eye, and at another spiral rotating in the opposite direction with the other eye this causes independent MAE’s from each eye separately but no MAE is seen when both eyes are open. MAE’s can result from the adaptation of either monocular or binocular neurons (Moulden, 1980; as cited in Antis & Duncan, 1983).
The fact that MAE’s can be mediated by monocular or binocularly driven neurons indicates MAE’s are the result of two separate pathways and that motion perception occurs in two parallel systems. Dichoptic MAE’s (caused when each eye is exposed to opposite directions of motion, either simultaneously or alternatively, the direction of the MAE is contingent on which eye views the stationary display). Dichoptic MAE’s are said to be caused by monoculary driven neurons. Alternatively MAE’s driven by binocular neurons show interocular transfer. (Wohlegemuth, 1911; as cited in Antis & Duncan, 1983).
Peripheral cells are responsible for dichoptic MAE’s and MAE’s that show interocular transfer are mediated by cells in the central level whereby both eyes converge onto the same neurons. Binocularly driven units recover more quickly from adaptation, therefore two units must be processing in parallel, if they were processing in a sequence then the Dichoptic MAE’s would disappear at least as soon as the interoculary transferred MAE’s because the central units would depend on the peripheral ones for input. (Favreau, 1976).
The tilt after effect (TAE) is when prolonged exposure to an orientated pattern affects the perceived orientation of a subsequently observed pattern. For adapting orientations of 0-50 degrees a vertical test appears to be repelled away from the adapter in orientation, the strongest effect occurring between 10-20 degrees. There is a smaller attraction effect with larger angles and the vertical test will appear rotated towards the adapter. The visual system has a tendency towards the ‘norms’ of spatial orientation, both horizontal and vertical. (Gibson and Radner, 1937; as cited in Paradiso, 1989).
In the visual system the retinal ganglion cells firstly encode information about the viewed stimulus (for example the wavelength), the striate cortex then performs additional processing of this information and then transmit it to the visual association cortex. (Carlson,) Most neurons in the striate cortex are sensitive to orientation, if a line is positioned in a cells receptive field the cell will respond only when the line is in a given position (at a specific orientation) Hubel and Wiesel (1962) referred to orientation selective cells with receptive fields organised in an opponent fashion as simple cells. Simple cells show inhibitory surround, a line at a given orientation would excite a cell if placed in the centre of the receptive field but inhibit if moved away. Another type of neuron, complex cells also best to a line of a particular orientation but did not show inhibitory surround, a line would continue to excite while it was in the receptive field. Hubel and Wiesel (1962) also proposed a model of orientation selectivity in the V1, visual signals are relayed from the retina to the V1 via the lateral geniculate nucleus (LGN) Neurons in the LGN have circularly symmetric receptive fields are so are not orientation selective, Orientation selectivity in the V1 could arise if LGN cells with collinear receptive field centres sent signals to the same V1 cell.
The orientation tunings of the TAE have been found to inconsistent with cells in the sub cortical visual pathway giving this effect a striate or extrastriate origin (Ware & Mitchell, 1974). The extrastriate cortex is in general highly binocular (Zeki, 1978; as cited in Paradiso et al, 1989)
There are two explanations for the TAE. Firstly that the adaptation stimulus fatigues cortical neurons. In the adapting phase cells fire that most prefer that orientation. When the test pattern is shown, the pattern of activity is centred on cells preferring that orientation. However some cells have become fatigued that were stimulated by the adapting pattern and so may respond less, this causes the pattern of neural activity to be shifted away from the adaptation orientation resulting in a tilt-after effect. (Kohler & Wallach, 1944) Alternatively, the TAE results from prolonged inhibition of orientation selective cells activated by the adaptation lines (Deutcsh, 1964 as cited in Paradiso)
Paradiso et al (1989) used the TAE to study interactions between real and subjective contours. Participants adapted to either real of illusory lines and were then shown test stimuli containing real or illusory lines. They found that interocular transfer of the TAE was greatest when the test stimulus was subjective than when it is real. They found that the perception of subjective contours was consistent with properties of the V2 neurons which known to be orientation selective and highly binocular.
The TAE, unlike the MAE shows complete interocular transfer (Campbell & Maffei, 1971). The channels that is responsible for orientation and spatial frequency are only partially transferred from one eye to the other (Blakemore & Campbell, 1969; as cited in Campbell & Maffei, 1971).
From the study of after effects we have learnt there are orientation selective cells in the visual cortex, these cells may be simple or complex. The prevailing theory for the TAE is based on lateral inhibitory interactions between orientation detectors in the primary visual cortex. The way in which cells respond to visual information is the key to how the brain processes visual information.
References
Antis, S & Duncan, K(1983) Separate motion aftereffects from each eye and from both eyes. Vision Research, 23(2) 161-169
Barlow, HB & Hill, RM(1963) Evidence for a physiological explanation of the waterfall phenomenon and figural aftereffects. Nature. London 225. 426-429
Carlson, N (2002) Foundations of Physiological Psychology. Boston: Allyn & Bacon.
Campbell, FW & Maffei(1971) The tilt after effect: A fresh look. Vision Research. 11, 833-840
Collman(2003) Oxford dictionary of Psychology. Oxford: Oxford University Press.
Favreu, O(1976) Motion aftereffects: Evidence for parallel processing in motion perception. Vision Research, 16, 181-186
Hubel, DH & Wiesel, T.N (1962) Receptive fields, binocular interaction and functional architecture in the cats visual cortex. Journal Of Physiology(London), 160:106-154
Mather, G, Verstraten, F & Anstis, S(1998) The motion aftereffect. London. MIT press.
Mollon, J(1974) After effects and the brain. New scientist. 479-482
Paradiso, M, Shimojo, S & Nakayama, K(1989) Subjective contours, tilt aftereffects and visual cortical organisation. Vision Research. 29(9) 1205-1213
Ware & Mitchell(1974) On Interocular Transfer of Various Visual
After-Effects in Normal and Stereoblind Observers, Vision Research, 14, 732-734
