1. In experiments examining the possibility that an excitatory amino acid may be an optic nerve transmitter in mammals, excitatory amino acid antagonists have been ionophoretically applied to cells in layers A and A(1) of the cat dorsal lateral geniculate nucleus and their effect on the excitatory response to visual stimulation of the receptive field centre has been assessed.2. The antagonists used were D-alpha-aminoadipate (D-alpha-AA), DL-alpha-epsilon-diaminopimelic acid (DAP), 1-hydroxy-3-amino-2-pyrrolidone (HA-966) and L-glutamate diethyl ester (GDEE). The antagonist effects on the visual response were compared with their effect on similar magnitude responses evoked by ionophoretic pulses of selected agonists and a control excitant, generally acetylcholine.3. Both D-alpha-AA and HA-966 would selectively block or depress the visual response with respect to the response to the control excitant. At the stage the visual input was blocked, responses to the agonists N-methyl-D-aspartate (NMDA), DL-homocysteic acid (DLH) and glutamate were also greatly reduced or blocked. At dose levels below those causing a significant reduction in the visual response, D-alpha-AA and HA-966 would selectively depress responses to NMDA and DLH with respect to the response to glutamate.4. GDEE was relatively ineffective in blocking either agonist responses or the visual response and only produced a significant reduction in either at dose levels that caused a similar depression in the response to acetylcholine. DAP would block responses to DLH but produced no significant effect on the visual response or the responses to glutamate and acetylcholine.5. The cholinergic antagonists atropine and dihydro-beta-erythroidine (DHbetaE) blocked responses to acetylcholine without significantly reducing either visual driving or the response to DLH.6. The effects were the same for X and Y cells in the dorsal lateral geniculate nucleus (dLGN). There was also no distinctions between ;on' and ;off' centre types of each of the two groups.7. The significance of these results is discussed. It is argued that they reintroduce the possibility that either L-aspartate, L-glutamate or a similar substance may be the transmitter mediating the optic nerve input to the cat dLGN.