Epileptic foci were established by application of Na-penicillin on the exposed parietal cortex of rats (n = 66) anesthetized with pentobarbital. Spikes appearing after a brief (greater than 30s) spontaneous interruption of the interictal discharge were sometimes followed by a spike-triggered spreading depression (STSD) wave, which blocked the activity of the focus for several min. The first recovering spike induced another STSD and repetitive STSD generation continued for up to 20 cycles, with a median cycle duration of 6 min. STSDs appeared more regularly after postictal depression induced by electrical stimulation of the focus or of the symmetrical brain area, and could also be elicited by SD waves evoked by microinjection of 5% KCl into extrafocal cortical regions. An ongoing STSD cycle was interrupted when another penicillin focus in the contralateral hemisphere started to trigger the focal discharge during relative SD refractoriness. STSD waves were observed in 42% of the animals. Attempts to elicit STSD were successful in 70% when the interictal discharge rate was low (less than 10/min) but mostly failed with higher discharge rates (greater than 30/min). It is suggested that STSD is generated when an isolated epileptic spike appears at the level of decreased potassium clearance and that repetitive STSDs are produced by synaptically and metabolically mediated interaction between focal discharge and spreading depression.

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Slow potential recording was used for longterm monitoring of the penumbra zone surrounding an ischemic region produced by middle cerebral artery (MCA) occlusion in adult hooded rats (n = 32). Four capillary electrodes were chronically implanted at 2-mm intervals from AP -3, L 2 (El) to AP 0, L 5 (E4). Spontaneous or evoked slow potential waves of spreading depression (SD) were recorded during and 4 h after a 1-h MCA occlusion and at 2-to 3-day intervals afterward for 3 weeks. Duration of the initial focal ischemic depolarization was maximal at E4 and decreased with distance from the focus. SD waves in the penumbra zone were high at El and E2, low and prolonged at E3, and almost absent at E4. Amplitude of elicited SD waves was further reduced 3 days later and slowly increased in the following week. Cortical areas displaying marked reduction of SD waves in the first days after MCA occlusion either remained low or showed substantial (60%) recovery, the probability ofwhich decreased with the duration of the initial focal ischemic depolarization and increased with the distance from the focus. It is concluded that the outcome of ischemia monitored by long-term SD recovery in the perifocal region can be partly predicted from the acute signs ofMCA occlusion.Research into Leao spreading depression (SD) (1), a selfpropagating neurohumoral reaction mediated by release of potassium ions and excitotoxic amino acids from depolarized areas of cerebral cortex, has always been tightly related to studies of electrophysiological manifestations of brain anoxia or ischemia (2, 3). The anoxic depolarization (AD) (4)