Abstract
Two mechanisms are discussed which link extracellular potassium accumulation and epileptogenic neuronal hyperactivity in the cortex. The potassium concentration (aK) of the environment of a repetitively discharging membrane can increase sufficiently for a supra-threshold depolarization at afferent erminals. This can explain the finding of ectopic spike generation and the antidromic breakthrough in thalamo-cortical projections after a primary cortical discharge. Spread and recurrent enhancement of excitatory drives may be the result of this mechanism. Initiation and termination of seizure is not explained by potassium accumulation. There is a ceiling level in potassium of about 10 mequ/1 which is strictly maintained during normal as well as epileptiform activity. This level is probably not high enough for depolarizing inactivation of neuronal membranes. Stimulation of cortical afferents can have a dual effect on aK. After a primary shortlasting increase, aK can reach subnormal values. This is possibly brought about by a stimulated re-uptake of K+. Seizures can be initiated at these subnormal levels. The effect of the re-uptake e.g. hyperpolarization of terminal afferents and increase of evoked transmitter release is discussed for the initiation for paroxysmal activity.
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