Our initial efforts to detect and analyze single neurons in the cortex were unsatisfactory for the purposes of an analyzing the effects of ischemia and cold lesions to the cortex. Improved success followed comparison of power spectra of occipital and frontal EEG in the rat subjected to a parietal cold lesion. Normally, the dominant frequency was about 5 Hz with higher frequency components. Rats subjected to a parietal cold lesion showed immediate reduction in EEG amplitude and loss of high frequency components. The dominant frequency in power spectrum analysis of the EEG showed a shift to l-3Hz and remained there for more than 1 week of animal survival. The amplitude, however, recovered rapidly within about 20 minutes. Visually evoked potentials were also examined using flash stimulation and extradurally placed electrodes over visual area 1. The cold lesions were applied as in the aforementioned lesions. A most striking result was a reduction of latency, starting at about 4 hours and reaching a maximum at 24 hours to 3 days. On the assumption that this reflected heightened excitability from excessive presence of glutamate, a non-competitive antagonist of glutamate, MK-801 was given intraperitoneally (2 mg/kg) at 24 hours after the cold lesion. The effect of this treatment was a prolongation of the latency beginning within about 5 minutes of injection and lasted about 4 hours. This was associated with a marked reduction of amplitude of the evoked response. This effect of a direct application of glutamate (IM) resulted in reduction of latency, similar to the cold lesion..This provides further support to the hypothesis that glutamatergic mechanisms were involved in the generation of the evoked response.
