The question arises if the visual signals arriving via feedback cortico-cortical connections can per se drive the spike-activity of cortical neurons. There is a clear evidence that in the cat, transient reversible inactivation of small volume of layer A of LGNd results in virtual silencing of simple and complex cells in area 17 whose RFs are in the precise retinotopic alignment with the center of GABA injections into the LGNd (Martinez and Alonso, 2001). On the other hand, when direct input from layer A of LGNd is reversibly blocked, the visuotopically corresponding part of cat’s area 18 is able to provide effective excitatory feedback drive to the supragranular layers of area 17 (Mignard and Malpeli, 1991). Overall, relatively selective removal of the feedback input from the higher-order cortical areas, without removing the other channels through which the visual input can reach a cortical neuron, might render the neuron unresponsive to visual stimuli. Thus, some of our area 19 neurons ceased to respond to visual stimuli when almost entire ipsilateral PTV cortex has been selectively inactivated, and their responsiveness to visual stimuli was restored when PTV was rewarmed. Similarly, when the entire ipsilateral area 18 (V2), rather than only the part corresponding visuotopically to the regions in V1 recorded from, was inactivated, some V1 neurons ceased to respond to visual stimuli (Sandell and Schiller, 1982). Their responsiveness to visual stimuli was restored when V2 was rewarmed (Sandell and Schiller, 1982).