Visual motion detection in man is governed by non-retinal mechanisms.

It is generally assumed that there is no sizable proportion of motion detectors in the primate retina. To test this specifically for humans, visual evoked potentials (VEPs) and electroretinograms (ERGs) were recorded simultaneously to visual motion onset (9.3 degrees /s) of an expanding or contracting 'dartboard'. The degree of motion-specific responses in cortex and retina was assessed by testing the direction specificity of motion adaptation with three conditions in a fully balanced paradigm: motion-onset potentials were measured after adaptation to: (1) a stationary pattern; (2) motion in the same direction as the test stimulus; and (3) motion in the opposite direction. Motion-onset responses in the VEP were dominated by the typical N2 at 150 ms, in the ERG by a positivity at 70 ms. Onset of contraction or expansion evoked virtually identical VEP and ERG responses (P>0.5). Motion adaptation produced strong direction-specific effects in the VEP (P<0.05), but not in the ERG (P=0.58): In the adapting and non-adapting direction the VEP (N2) was reduced by 75 and 50% (P<0.001), the ERG by 32 and 26% (P<0.01 and 0.05), respectively. The striking difference of the direction-specificity of motion adaptation between cortex and retina suggests that in humans the vast majority of motion-specific processing occurs beyond the retinal ganglion cells.