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Sensitivity to differential motion components, shearing and compressive (opposed) motion, was examined. The hypothesis that the visual system contains local mechanisms specifically sensitive to these types of motion was tested. Stimuli consisted of two moving sinusoidal gratings. Sensitivity to shear and compression was compared with sensitivity for linear motion. Lower thresholds of motion and contrast sensitivities were obtained. Subjects were more sensitive to opposed than to non-opposed motion for a range of grating orientations and different grating spatial frequencies. However sensitivity for opposed motion decreased in the presence of a second added linear motion. The hypothesis of local shear and compression mechanisms was rejected in favour of antagonistic (opponent) interactions between local motion mechanisms. Motion capture was examined. Stimuli were made up of a circular test grating surrounded by another grating. Subjects were required to judge the direction of motion of the test grating. Experiments examined the effects on motion capture of: centre grating size; orientation of surround; relative contrast of centre and surround; plaids in the surround. Conditions favouring motion capture were: with the smallest centre grating; with surround and centre orientations within thirty degrees; with surround had higher contrast than the centre; and only when a plaid surround contained a component of similar orientation as the centre. For conditions of motion capture relative to those of no-capture, increased velocity thresholds for judging the centre direction were found. This was associated with a shift in the bias point between opposed directions with no change in overall sensitivity to motion. It is suggested that a cooperative network of local motion mechanisms featuring centre-surround opponency can account for all the results of this study.

No / Physiological studies of colour vision have not yet resolved the controversial issue of how chromatic opponency is constructed at a neuronal level. Two competing theories, the cone-selective hypothesis and the random-wiring hypothesis, are currently equivocal to the architecture of the primate retina. In central vision, both schemes are capable of producing colour opponency due to the fact that receptive field centres receive input from a single bipolar cell ¿ the so called `private line arrangement¿. However, in peripheral vision this single-cone input to the receptive field centre is lost, so that any random cone connectivity would result in a predictable reduction in the quality of colour vision. Behavioural studies thus far have indeed suggested a selective loss of chromatic sensitivity in peripheral vision. We investigated chromatic sensitivity as a function of eccentricity for the cardinal chromatic (L/M and S/(L + M)) and achromatic (L + M) pathways, adopting stimulus size as the critical variable. Results show that performance can be equated across the visual field simply by a change of scale (size). In other words, there exists no qualitative loss of chromatic sensitivity across the visual field. Critically, however, the quantitative nature of size dependency for each of the cardinal chromatic and achromatic mechanisms is very specific, reinforcing their independence in terms of anatomy and genetics. Our data provide clear evidence for a physiological model of primate colour vision that retains chromatic quality in peripheral vision, thus supporting the cone-selective hypothesis.