Discovering the neurotransmitters involved in the generation of flash evoked potentials (FEPs) would enhance the use of FEPs in screening for and assessment of neurological damage. Recent evidence suggests that the excitatory amino acids, glutamate and aspartate, may be transmitters in the visual system. Ketamine selectively antagonizes the actions of excitatory amino acids on n-methyl-d-aspartate receptors and may be administered systemically. The effects of ketamine (37, 75, 150 mg/kg) on FEPs recorded in light and dark backgrounds were investigated. Ketamine administration resulted in dose dependent alterations in FEP peak amplitudes and latencies. Peak P1 amplitude increased by a factor of 4, in a dose dependent manner. Peak N1 virtually disappeared at 150 mg/kg. Peak P2 amplitude increased by 50%, but only in the light background, and only at 150 mg/kg. Ketamine (150 mg/kg) effect on peak P1 and peak N3 amplitudes were maximal 5 min after ketamine administration, but were not recovering 30 min post-injection. The various peak latencies were also affected differently. The results suggest that glutamate or aspartate is involved in the generation of the rat FEPs.