Small amounts of penicillin were used to create a seizure focus in the primary visual cortex (area 17), extrastriate cortex (area 18 and 18a), and neighboring somatosensory and temporal areas in rats. Autoradiography with 14C-deoxyglucose was used to map the focus and the local cortical and long subcortical circuits. Mild seizures from area 17 were associated with focal spiking without behavioral manifestations. There was restricted utilization of local U-fiber circuits and ipsilateral subcortical visual system nuclei. Stronger seizures filled up the visual cortex and projected into adjacent neocortex and limbic cortex, the contralateral 17–18a border, and additional subcortical nuclei. Seizures originating in the posterior visual cortex were associated with prolonged afterdischarges and stereotyped behavioral manifestations, with spread into the posterior cingulum, the subicular complex, and the bilateral hippocampus. After analyzing the eleetrographic discharges, behavior, and seizure pathways in each animal, we conclude that ictal symptoms associated with seizures would not be the expression of the function of a cortical focus, but rather of the dysfunction of excessive discharges through many local and long circuits.