Abstract
The potassium ion plays a unique role in brain function since it is released from excited neurons to an extracellular space which, at least at several locations, is limited to clefts of 150 Å thickness 23, 53. Neuronal function can therefore be expected to evoke an increase in the extracellular potassium concentration, and such an increase has in recent years been convincingly demonstrated. The observed increase after ‘normal’ neuronal activity is relatively small, but during spreading depression the extracellular potassium concentration may reach such high levels as 60–80 mM29, 54. These concentrations are similar to the potassium concentrations of 30–100 mM which for years have been used for in vitro studies of potassium effects on energy metabolism and transport of amino acids, inorganic ions and water. The potassium effects are to a large extent mimicked by application of electrical stimulation, and they have often been assumed to be secondary to a potassium-induced depolarization. Another possibility is, however, that excess potassium might act by a direct stimulation of an ion-activated system, and there is no reason to take for granted that different effects by potassium are all evoked in the same way. A distinction between the various effects exerted by high concentrations of potassium may possibly be obtained by studying cellular and subcellular localization of the different phenomena as well as their ontogenetic development.
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Hertz, L. (1976). Potassium Effects on Transport of Amino Acids, Inorganic Ions, and Water: Ontogenetic and Quantitative Differences. In: Levi, G., Battistin, L., Lajtha, A. (eds) Transport Phenomena in the Nervous System. Advances in Experimental Medicine and Biology, vol 69. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-3264-0_27
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