High-intensity photocoagulator lesions placed nasally to the optic disc one eye destroyed all retinal layers and led to visual deafferentation of the lateral part of layer A in the contralateral lateral geniculate nucleus (LGN) of adult cats. The retino-geniculate topography was determined with vertical tungsten microelectrode penetrations through LGN layers A and A1 before and at different times after photocoagulation. Before the 20th day a border of light excitability was found in layer. A corresponding to the normal projection of the lesion onto the LGN. Deviations from the normal topographical organization were evident 30 days and later after photocoagulation. Cells were recorded within the deafferented part of layer A near to the border of deafferentiation which had receptive field (RF) centers displaced by more than two degrees of visual angle with respect to the normal retinotopy. During formation of the retinal scar no identifiable points on the retina were displaced in the same direction as the RF centers. The histological control of the retinal lesions proved that there was no potentially excitable tissue left to account for a spread of excitation into the lesion. Latency measurements after electrical stimulation of the optic tract and the visual cortex suggested a retinal input and a projection into the visual cortex for the LGN cells with displaced receptive field centers. RF center displacements up to five degrees at the border of the lesions indicated a lateral spread of excitation within the LGN up to 250 micron beyond normal.