Cerebral [K+]e increase as an index of the differential susceptibility of brain structures to terminal anoxia and electroconvulsive shock

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Abstract
The time course of the [K+]e increase elicited by terminal anoxia or by electroconvulsive shock (ECS) was compared in various parts of the rat brain. The [K+]e was measured with ion‐selective microelectrodes stereotaxically introduced into the target area. Respiration arrest induced in anesthetized rats a slow [K+]e increase to about 6–10 mM followed by an abrupt rise to 30–50 mM (doubling time 5–14 sec) in the neocortex, hippocampus, amygdala, caudate nucleus, and thalamus. In the reticular formation, zona incerta, and lateral hypothalamus the second phase of [K+]e increase was much slower (doubling time 30–50 sec) and lacked the autoregenerative character. Trans‐pinnate ECS (50 Hz, 0.5 sec, 80 mA), administered to rats immobilized with gallamine triethiodide, elicited a generalized [K+]e increase of the spreading depression type in neocortex and hippocampus (40 mM) as well as in the caudate nucleus and thalamus (20–30 mM), followed by slow [K+]e decrease (half‐time 40–60 sec). Much lower ECS‐induced [K+]e increase (to 5–6 mM) was observed in the reticular formation, zona incerta, lateral hypothalamus and, surprisingly, in the amygdala. It is concluded that the autoregenerative [K+]e release of spreading depression type develops in structures with high density of membranes reacting to partial depolarization by increased sodium permeability.