1. In nine 4‐week‐old, dark‐reared kittens we sutured one eye closed and rotated the other surgically. The kittens then grew up in a normally lighted animal colony with adequate room to play. 2. For about two weeks after surgery their visual‐motor co‐ordination did not differ from that of kittens with conventional monocular deprivation; then severe disturbance of visually guided behaviour became progressively more apparent until, after another two to three weeks, all the kittens stopped responding to most visual stimuli entirely. At that point their behaviour in an unfamiliar environment closely resembled that of binocularly deprived cats exposed to light for the first time. 3. Four weeks (n = 3) and 6 months (n = 6) after surgery, we examined the visual cortex with single‐unit recordings, and with evoked potentials elicited by electrical stimuli and patterned lights. We obtained the single‐unit recordings from 586 neurones of the striate cortex in both hemispheres, both ipsi‐ and contralateral to the deprived eye. 4. The single‐unit recordings and the evoked potentials showed a clear relation between the kitten's abnormal visual behaviour and the functioning of the striate cortex. Only about half the normal percentage of cells responded to light, and most of those which did react had abnormal receptive field properties: they responded only sluggishly even when the light stimuli were aligned optimally. 5. We also evoked cortical potentials with phase alternating square wave gratings of variable contrast and spatial frequency. The amplitude of the potentials indicated that contrast‐sensitivity was reduced at all spatial frequencies. 6. In the kittens tested 4 weeks after surgery, ocular dominance had shifted toward the open rotated eye but this shift was considerably less pronounced than in control kittens monocularly deprived for a comparable period of time. 7. In the kittens tested 6 months after surgery fewer cells than normal were binocular; ocular dominance had not shifted towards the open eye. 8. Numerous control experiments indicated that these abnormalities did not result from transitory immobilization of the eye alone nor from lesions of the retina or of the optic nerve. We infer that a central mechanism prevents the inappropriate signals from the rotated eye from influencing the consolidation of central pathways.