The cortical contribution to the orientation and direction sensitivity of LGNd relay cells was investigated by recording the responses of relay cells to drifting sinusoidal gratings of varying spatial frequencies, moving bars, and moving spots in cats in which the visual cortex (areas 17, 18, 19, and LS) was ablated. For comparison, the spatial-frequency dependence of orientation and direction tuning of striate cortical cells was investigated employing the same quantitative techniques used to test LGNd cells. There are no significant differences in the orientation and direction tuning to relay cells in the LGNd of normal and decorticate cats. The orientation and direction sensitivities of cortical cells are dependent on stimulus parameters in a fashion qualitatively similar to that of LGNd cells. The differences in the spatial-frequency bandwidths of LGNd cells and cortical cells may explain many of their differences in orientation and direction tuning. Although factors beyond narrowness of spatial-frequency tuning must exist to account for the much stronger orientation and direction preferences of cells in area 17 when compared to LGNd cells, the evidence suggests that the orientation and direction biases present in the afferents to the visual cortex may contribute to the orientation and direction selectivities found in cortical cells.

Patch-clamp recordings were made from ganglion cells in an in vitro dark-adapted rabbit retina preparation. Cells were stimulated by images generated on a computer monitor and focussed onto the photoreceptors. Excitatory inward currents were recorded in response to spot stimuli centered on the somas of the recorded cells. Center illumination of on-brisk-transient cells produced large transient excitatory postsynaptic currents (EPSCs) which were invariably followed by a small steady-state inward component. Illumination of a centered annulus failed to elicit the transient EPSC. Simultaneous illumination of the annulus and the center spot blocked the large transient EPSC, consistent with activation of an inhibitory surround. Application of tetrodotoxin (TTX), which blocks sodium-dependent action potentials, also blocked the surround inhibition in ON-brisk transient cells as well as some other classes of ganglion cells. It is concluded that, in some ganglion cell classes, the surround is generated largely through the activity of spiking neurons, and it is suggested that the amacrine cells in the inner plexiform layer are involved.