The sensitive period for strabismus in the kitten.
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Biomedical subjects
F B Levitt
Publications and source records attributed to F B Levitt.
Recovery of binocular function in kitten visual cortex.
1. This paper describes the results of an experiment designed to examine the ability of cells in the kitten's visual cortex to regain functional binocular connections following exposure to a brief period of visual deprivation. 2. Normal 4-wk-old kittens were exposed to a total of 12 h of optically induced strabismus over a period of 2 days, and single-unit recordings made the following day indicated that the proportion of striate cortex cells with binocular receptive fields had decreased sharply as a result of this episode of strabismic vision. 3. When these kittens were revived and allowed to experience a recovery period of normal binocular vision lasting either 3 or 7 wk, cortical binocularity returned to a normal level. 4. Statistical analysis revealed that the difference in the level of binocularity observed before and after the period of binocular recovery was highly significant, and comparison of the results from kittens allowed only a 3-wk recovery period with those from kittens allowed a 7-wk period indicated that a similar level of recovery was obtained in each group. 5. Histological reconstruction of electrode penetrations indicated that the recovery of binocular receptive fields occurred uniformly across all cortical laminae. 6. These data are discussed in terms of the results from previous recovery experiments, the relationship between cortical binocularity and the ability to maintain binocular fixation, and the possibility that subliminal cortical input plays a role in the recovery of functional binocular cells.
Animals↗
Experimental strabismus in the kitten.
1. We have examined the relative roles of visual and nonvisual input to striate cortex cells in causing the breakdown of binocularity produced by brief periods of visual-axis misalignment in kittens. 2. In the first study, the binocularity of single neurons recorded from the striate cortex was assessed in kittens reared with either surgical or optical strabismus. Surgical strabismus was induced by performing a unilateral medial rectus tenotomy, and optical strabismus by means of goggles that held prisms of equal power before the two eyes with their bases oriented in opposite directions. The loss of functional binocular connections was of comparable severity in these two groups of kittens. Control kittens, reared wearing goggles containing prisms whose bases were oriented in the same direction, showed normal levels of binocularity. 3. In the second experiment, normal kittens were given a surgical strabismus at around 1 mo of age and kept in total darkness for 2 days, 2 wk, or 4 wk. Cortical binocularity was normal in these kittens. 4. Finally, a group of kittens was reared in the illuminated colony with a symmetric surgical strabismus (bilateral medial rectus tenotomy). These kittens suffered a severe loss in cortical binocularity that was comparable to that seen in control kittens reared with asymmetric (unilateral) strabismus. 5. We conclude that altered visual input caused by misregister of the images falling in the two eyes is necessary and almost certainly sufficient to cause breakdown of cortical binocularity in kittens exposed to brief periods of divergent strabismus and that, when strabismus is induced surgically, this loss of binocularity is not dependent on the symmetry of the surgical manipulation; we thus find no evidence for a special role of afferents from the extraocular muscles in producing this effect.
Animals↗
Altered visual experience reduces cortical binocularity in strabismic kittens.
We have studied the relative importance of visual and nonvisual signals to striate neurons in causing the loss of cortical binocularity that occurs when young kittens are subjected to brief episodes of stabismus. In kittens kept in a normally illuminated colony, the reduction in binocularity was the same whether the strabismic was induced optically or surgically. When surgically strabismic kittens were kept in total darkness, cortical binocularity was unchanged. We conclude that anomalous visual input is both necessary and sufficient to cause loss of binocularity in strabismic kittens and that nonvisual (proprioceptive) input from the orbit has no part in producing this effect.
Animals↗