OBJECTIVE The monkey photopic ERG was studied during administration of glutamate analogs to determine whether the photopic a-wave derives exclusively from photoreceptors. METHODS Monkey photopic ERGs were elicited using 200-msec flashes or 30-microseconds xenon photostrobe flashes on a steady light-adapting background of 40 cd/m2 (3.3 log scotopic troland). Intravitreal injections of APB, PDA, or both were given to block transmission to depolarizing and hyperpolarizing second-order retinal neurons, respectively. RESULTS After injecting PDA to block light responses of horizontal cells and hyperpolarizing bipolar cells, part of the photopic a-wave was eliminated. The PDA-sensitive component, presumed to be due to activity postsynaptic to cones, was responsible for the photopic a-wave threshold and dominated the response over the initial 1 to 1.5 log units of intensity. For brighter stimuli, this component made a constant contribution to the photopic a-wave. A non-PDA-sensitive contribution to the a-wave, presumed to originate directly from cones, was first evident 1 to 1.5 log units above photopic a-wave threshold. It progressively dominated the a-wave at higher intensities, particularly at early time points after the flash. Injecting PDA almost eliminated the photopic a-wave elicited with bright xenon photostrobe flashes that are commonly used for human clinical ERG diagnostic testing, indicating that this a-wave may contain significant postreceptoral activity. CONCLUSIONS The primate photopic ERG a-wave derives, in part, from retinal activity postsynaptic to cone photoreceptors, particularly for stimuli near the photopic ERG threshold that are typically used for human clinical studies.