Ketamine alters rat flash evoked potentials.

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. Two experiments were designed to test the effects of ketamine on rat FEPs. First, the effects of ketamine (37, 75, 150 mg/kg) on FEPs recorded in light and dark backgrounds were investigated at a single (10 min) posttreatment interval. 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. Second, ketamine (150 mg/kg) effects on FEPs were investigated 5 min and 30 min following administration. The decrease in peak N1 amplitude was maximal 5 min after administration and the amplitude was recovering at 30 min. The effects on peak P1 and peak N3 amplitudes were maximal 5 min after ketamine administration, but were not recovering 30 min postinjection. The various peak latencies were also affected differently. The possible role of glutamate or aspartate in the generation of rat FEPs is discussed.