Abstract
The parameters of cortical electrical stimulation (ES) producing synaptically-operated spreading depression (SD) were determined in rats. Waves of SD were regularly triggered in the thalamus by brief, high frequency ES (0.02–0.05 sec; 200–500 Hz) of the parietal cortex. Monitoring by EEG confirmed the lack of accompanying convulsive activity in the cortex and the subcortical structures investigated. Use of Nembutal-induced anesthesia led to a higher minimum threshold for onset of SD, without preventing short-latency thalamid SD. Stimulating the parietal cortex was less effective for synaptic excitation of hippocampal and caudate SD. Hippocampal, unlike thalamic SD, was accompanied by spells of epileptiform activity, most pronounced at certain points in the onset and decline of the SD wave. These brief convulsive episodes were not the cause but the result of SD to a large extent. The low, subconvulsive threshold of synaptically triggered subcortical as well as cortical structures should therefore be taken into account when considering the functional significance of the SD reaction.
Published Version
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