The ocular dominance distribution and the excitability level of single cells in the callosal projection zone of the visual cortex (area 17-18 boundary), were electrophysiologically studied in acute and in chronic cats following simultaneous (OCX-CCX) and separate transections of the optic chiasm (OCX) and corpus callosum (CCX). Except for a few cells (3.4%) in the acute OCX-CCX cats showing an interhemispheric transfer, as expressed by their contralateral eye response, all other cells had a monocular response to the ipsilateral eye. An ipsilateral monocular response was found in the chronic OCX-CCX cats, even for long survival periods (17.0 months). The result for the OCX cats was similar, as indicated by the major ipsilateral response and the small proportion of cells showing an interhemispheric transfer. No improvement was found with postoperative time; acute OCX cats had 5.0% cells with contralateral input and 1-7 months chronic cats had 1.7-6.5% of these cells. These animals have thus split brain from point of view of the visual cortex; each hemisphere is therefore independent of the other one as far as neuronal functions are concerned. A remarkable reduction in binocularity was found following callosal transection (CCX) both in acute (41.4% binocularly driven cells) and in 3-39 months chronic cats (45.5% cells), in comparison to the control cats (74.2%). This indicates that elimination of the corpus callosum as itself enhances the binocularity diminution in split brain cats. The reduction found in visual responsiveness in our split brain cats (total: 63.2% unresponsive cells), is attributed to the summation of the individual effects of the optic chiasm and corpus callosum transections. A consistent tendency was found in the long chronic in comparison to the acute OCX-CCX, OCX, and CCX cats for a decrease in the responsiveness level with survival time; however, the short chronic OCX-CCX and CCX cats had the maximal proportion of unresponsive cells. It was concluded that the split brain induced in adult cats has a permanent effect on interhemispheric transfer to visual cortex cells. The absence of interhemispheric interaction under these conditions is not compensated by either transfer through anterior parts of the corpus callosum or through other commissures.