BEFORE A KITTEN OPENS ITS EYES, and long before the eyes are used in visual exploration, single cells of the primary visual cortex respond to natural stimulation with the same specificity as is found in the adult (5). This suggests that the anatomical connections between retina and striate cortex are for the most part innate. During the first 3 months of life the connections are highly susceptible to the effects of visual deprivation, to the extent that exclusion of all form and some light from one eye leads to a severe decline in the ability of that eye to influence cortical cells. Anatomical and physiological evidence suggests that the defect is chiefly, though not entirely, a cortical one (7-9). The object of the present study was to influence cortical connections by some means less drastic than covering one or both eyes. We wished if possible to alter the input in such a way that there would be no question of effects on the visual pathway below the level of the striate cortex. A method was suggested by the well-known clinical observation that a child with a squint (strabismus or nonparallel visual axes) may suffer a deterioration of vision in one eye (amblyopia ex anopsia). Since the visual pathways from the two eyes are for practical purposes separate up to the level of the striate cortex, it is unlikely that in these children the defect is in the retina or geniculate. An artificial squint therefore seemed to provide a possible means of obtaining a cortical defect while sparing the retina and lateral geniculate body. Accordingly , we produced a divergent strabismus by cutting one of the extraocular muscles in each of four newborn kittens, with the plan of testing vision and recording from single cortical cells after several months to a year. When at length each eye was tested in these kittens by observing the ani-mal's behavior with the other eye covered the results were disappointing: there was not the slightest suggestion of any defect in vision in either eye. This was not entirely unexpected, since with both eyes uncovered the animals had appeared to fix at times with one eye and at times with the other. At this stage there seemed to be little point in proceeding further, for there- .
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Single unit activity in striate cortex of unrestrained cats
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1959,
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Receptive fields of single neurones in the cat's striate cortex
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1959,
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Receptive fields, binocular interaction and functional architecture in the cat's visual cortex
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1962,
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D. Hubel,et al.
RECEPTIVE FIELDS OF CELLS IN STRIATE CORTEX OF VERY YOUNG, VISUALLY INEXPERIENCED KITTENS.
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1963,
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D. Hubel,et al.
EFFECTS OF VISUAL DEPRIVATION ON MORPHOLOGY AND PHYSIOLOGY OF CELLS IN THE CATS LATERAL GENICULATE BODY.
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1963,
Journal of neurophysiology.
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D. Hubel,et al.
SINGLE-CELL RESPONSES IN STRIATE CORTEX OF KITTENS DEPRIVED OF VISION IN ONE EYE.
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1963,
Journal of neurophysiology.
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Shape and arrangement of columns in cat's striate cortex
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1963,
The Journal of physiology.
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Extent of recovery from the effects of visual deprivation in kittens.
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1965,
Journal of neurophysiology.
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D. Hubel,et al.
Comparison of the effects of unilateral and bilateral eye closure on cortical unit responses in kittens.
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1965,
Journal of neurophysiology.
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D H HUBEL,et al.
RECEPTIVE FIELDS AND FUNCTIONAL ARCHITECTURE IN TWO NONSTRIATE VISUAL AREAS (18 AND 19) OF THE CAT.
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1965,
Journal of neurophysiology.