Early efforts to detect and analyze the effects of injury in single neurons of the cortex following transient ischemia or cold lesion were unsatisfactory. Some success in detecting change became evident in examining power spectra of the EEG. The postischemic EG showed a shift of the dominant frequency from about 5HZ to 1-3 HZ and remained for more than 1 week. Visually evoked potentials clearly showed pronounced reduction in latency of 5-9 msec. Within 4-6 hours after placement of the cold lesion, the latency on the lesioned side began to decrease reaching 37+ 2 msec in 1-3 days. A similar reduction was observed in gerbils following transient ischemia by occlusion of the common carotid arteries. These shortened values were stable for more than the 2 hours that they were monitored. This reduction of latency in the visually evoked pathway is interpreted as evidence of hyperexcitability. Further support for this view was given by our finding that the reduced latency was quickly abolished by the administration of MK-801, and that a similar effect was produced by a direct application of glutamate to the exposed cerebral cortex.
