Single unit response latencies in striate cortex after visual stimulation with stationary flashed bars were measured and interocularly compared in anaesthetized cats with surgically induced strabismus, in order to elucidate the neural basis of strabismic amblyopia. Four unilateral esotropic and two exotropic cats were studied. The visual onset latencies of cortical neurons ranged from 30 to 170 ms after stimulation of the non-deviating eye at a contrast of 82%. Responses after visual stimulation of the deviating eye were consistently delayed by approximately 10 ms. The latency increase was independent of the direction and absolute angle of squint in the different animals. Peak latencies of cortical neurons ranged from 43 to 245 ms. Median peak latency was 85 ms for the non-deviating and 95 ms for the deviating eye. The rise time of cortical flash responses, as determined from onset-peak differences, ranged between 2 and 170 ms. Direct interocular comparison of response latencies in the remaining binocular neurons revealed an invariable advantage for the non-deviating eye. Supragranular neurons showed a greater interocular latency difference than neurons in layer IV. Visual latencies were contrast-dependent. However, the latency reduction with increasing contrast was less pronounced for the deviating eye. We discuss the possibility that central integration times, especially within cortex, are prolonged in strabismic cats, affecting temporal coincidence of signal processing in the visual cortex. The resulting disturbance of spatio-temporal integration, as caused by a scrambling of geniculo-striate and intracortical connections, may be the substrate of binocular suppression and strabismic amblyopia.