One of the remarkable features of vision is that the perceived colour of reflecting surfaces which form part of complex, multicoloured scenes, remains stable despite large variations in the spectral composition of the illuminating light1–5. The phenomenon of colour constancy has long been known but only recently have electrophysiological studies revealed a possible mechanism for it in an area of visual cortex, the V4 complex in the rhesus monkey. Lesions in the V4 complex of experimental animals6,7 have produced little if any impairment of wavelength discrimination, but colour constancy has not been tested. In the present study we used a broader range of behavioural tasks, including one of colour constancy, to test the prediction that ablation of the V4 complex leads to selective deficits in colour perception. The results support the notion that the V4 complex is necessary for colour constancy but not for the discrimination of hue.

The common laboratory chemical, acrylamide, causes various clinical effects including dysfunction of the visual system. Previous electrophysiological recordings from the rat lateral geniculate nucleus (LGN) following exposure to acrylamide suggested that X-like cells were selectively disrupted by the neurotoxin. This study examines the possibility that the diameter of the optic tract fibres may underlie their differential susceptibility, but shows that fibres of all sizes are affected by acrylamide intoxication and the results suggest that the selective effect of acrylamide is not due simply to disruption of optic tract fibres.