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.