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Kaliumaktivität im Cortex der Katze: Untersuchungen zur experimentellen Epilepsie

Potassium activity in cortex: Studies on epileptogenesis

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Summary

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 terminals. 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 of paroxysmal activity.

Zusammenfassung

Zwei Wirkungszusammenhänge werden behandelt, die Kaliumakkumulation und epileptogene neuronale Hyperaktivität verbinden. Die K-Konzentration (aK) an einer repetitiv entladenden Membran kann genügen, um diese beträchtlich zu depolarisieren und Erregungen von afferenten Fasern und Synapsen hervorzurufen. K-Akkumulation kann ektopischen Erregungsvorgängen (Gutnick & Prince, 1972) und einem antidromen Erregungseinbruch in thalamo-cortikale Afferenzen nach einer vorausgehenden cortikalen Entladung zugrunde liegen. Krampfausbreitung und Verstärkung läßt sich durch einen rekurrenten Erregungszustrom erklären. Im erregbaren Cortex ist ein maximales aK von 10 mequ/1 zu finden, das auch während epileptiformer Aktivität nicht überschritten wird. Dieser Kaliumspiegel ist nicht ausreichend, neuronale depolarisierende Inaktivierung und demnach das Erampfende einzuleiten.

Erregung cortikaler afferenter Fasern kann duale Wirkung auf aK zeigen. Es werden durch Erregung häufig subnormale Werte des extrazellulären aK gefunden, die möglicherweise durch eine aktivierte Reabsorption von Kalium hervorgerufen werden. Epileptiforme Entladungen können durchaus auch bei subnormalem aK beginnen. Mögliche Effekte der K-Reabsorption, z. B. eine Hyperpolarisation terminaler Afferenzen und Anstieg evozierter Transmitterfreisetzung werden diskutiert im Hinblick auf den Befund initial verstärkter synaptischer Erregungsvorgänge während paroxysmaler neuronaler Entladungstätigkeit.

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  1. Abteilung Neurophysiologie, Max-Planck-Institut für Psychiatrie, Kraepelinstraße 2, D-8000, München 40, Bundesrepublik Deutschland

    Hans Dieter Lux

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  1. Hans Dieter Lux
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Herrn Professor Dr. med. Gerd Peters zu seinem 70. Geburtstag gewidmet.

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Lux, H.D. Kaliumaktivität im Cortex der Katze: Untersuchungen zur experimentellen Epilepsie. Arch. F. Psychiatr. U. Z. Neur. 221, 227–244 (1976). https://doi.org/10.1007/BF00418482

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