Abstract
Strabismic humans usually experience powerful suppression of vision in the nonfixating eye. In an attempt to demonstrate physiological correlates of such suppression, we recorded from the primary visual cortex of cats with surgically induced squint and studied the responses of neurons to drifting gratings of different orientation, spatial frequency, and contrast in the two eyes. Only 1 of 50 apparently monocular cells showed any evidence of remaining, subliminal excitatory input from the “silent” eye when the two eyes were stimulated with gratings of similar orientation, and even among the small proportion of cells that remained binocularly driven, very few exhibited facilitation when stimulated binocularly. The majority of cells from both exotropes and esotropes, even those that could be independently driven through either eye, displayed nonspecific interocular suppression: stimulation of the nondominant eye with a drifting grating of any orientation depressed the response to an optimal grating being presented to the dominant eye. This phenomenon exhibited a gross nonlinearity in that it was dependent on the temporal sequence of stimulus presentation: stimulation of the nondominant eye caused significant suppression only if the neuron was already responding to an appropriate stimulus in the dominant eye, but not when onset of stimulation in the two eyes was simultaneous. Interocular suppression was always independent of the relative spatial phase of the two grating stimuli, and usually broadly tuned for the spatial frequency of the suppressive stimulus. Suppression may depend on inhibitory interaction between neighboring ocular dominance columns, combined with the loss of conventional disparity-selective binocular interactions for matched stimuli in the two eyes. The similarity of interocular suppression in strabismic cats and that caused by orthogonal gratings in the two eyes in normal cats (Sengpiel and Blakemore, 1994; Sengpiel et al., 1994) suggests that strabismic suppression and binocular rivalry depend on similar neural mechanisms.