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

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.