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The present study examined the effects of Dizocilpine (MK-801; a noncompetitive N-methyl-D-aspartate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and superior colliculus (SC) of chronically implanted hooded rats. The potentials were recorded at 5, 20, and 35 min following i.p. injections of saline, and of 0.1, 0.3, and 1.0 mg/kg MK-801 on separate days. The amplitude of VC component P1 was unaltered following drug treatment. N1 was increased in amplitude by the 0.1-, 0.3-, and 1.0-mg/kg doses, while two other negative peaks in the VC emerged, beginning with the 0.1-mg/kg dose, to complicate the waveform. One negative peak developed between N1 and P2, while the other effectively split peak P2 (forming P2A and P2B). P2A was depressed at all doses, while P2B was depressed at 0.1 mg/kg but augmented at the 1.0-mg/kg dose. N2 was elevated by the 0.3- and 1.0-mg/kg doses, while P3 was increased in amplitude by all doses. N3 was transiently enhanced by the 0.3-mg/kg dose. SC amplitudes were less affected, with P3 and N4 reduced in amplitude by the 0.3- and 1.0-mg/ kg doses. The latencies of most components in both structures were decreased, often with all doses, but generally at the later recording times. A second experiment demonstrated significant MK-801-induced hyperthermia at all of the above doses, although a higher dose of 3.0 mg/kg MK-801 caused hypothermia. The reduction in component latencies may, therefore, result at least in part from a drug-induced hyperthermia. A third experiment demonstrated MK-801-induced changes in locomotor activity in rats in an open field. The effects were both dose and time dependent. The 0.3-mg/kg dose of MK-801 produced significant increases in the number of line crossings from 20-60 min in comparison to the saline condition. Increases in the number of line crossings with the 1.0-mg/kg dose peaked at 15 min, and then gradually declined. It is unlikely, however, that these changes in movement can account for the effects of MK-801 on evoked potentials. In conclusion, the results show that blockade of the ion channel associated with the NMDA receptor produces profound changes in the activity of the neural pathways that are reflected in the middle components of the flash-evoked potential recorded from the VC.

The effects of ketamine on locomotion in an open-field were determined in hooded rats. Animals were given intraperitoneal injections of saline, or of 1, 10, 50 or 100 mg ketamine/kg body weight on separate days. Open-field behavior was examined for 60 min following injection. The 50 mg/kg dose of ketamine produced an increase in locomotion which peaked approximately 30 min after injection. A cataleptic immobility produced by the 100 mg/kg dose was followed by postanesthetic locomotion. The ketamine-induced locomotion consisted largely of ambulation about the perimeter of the field and was accompanied by ataxia, but included relatively little tight circling (rotation) during the peak of activity. Comparisons with the results of past research suggests that test-chamber design influences the type of locomotion induced by ketamine.