The electrophysiological responses of 162 tectal cells to computer-generated visual stimuli were extracellularly recorded from 24 homing pigeons before and after injecting either lidocaine or N-methyl-D-aspartate (NMDA) into the nucleus isthmi pars magnocellularis (Imc) or the nucleus isthmi pars parvocellularis (Ipc). Micro-injections of lidocaine into Imc resulted in a significant reduction of firing rate in 80% of tectal cells, whose excitatory receptive fields (ERFs) were localized within the ERF of the Imc cell where the lidocaine was injected. In contrast, when lidocaine was injected into Ipc under identical circumstances it had no effect on the visually driven activity of 68% of tectal cells. However, when the excitatory amino acid NMDA was injected into Ipc it produced a significant reduction in the visually driven firing of 75% of tectal neurons when their ERFs were within the isthmic ERF, while similar application of NMDA into Imc had no effect on the visually driven response of 94% of tectal neurons. When the ERFs of tectal cells were localized outside the ERF of the isthmic cell where the chemical was injected, Imc-injected lidocaine had no effect in 9 out of 10 tectal cells, whereas Ipc-injected NMDA increased firing in 7 out of 17 tectal cells. Therefore, it is suggested that the Imc-tectal fibers participate in a positive feedback pathway and the Ipc-tectal fibers are involved in a negative feedback pathway.