Activity-Dependent Fluctuations in Interstitial [K(+)]: Investigations Using Ion-Sensitive Microelectrodes

In the course of action potential firing, all axons and neurons release K(+) from the intra- cellular compartment into the interstitial space to counteract the depolarizing effect of Na(+) influx, which restores the resting membrane potential. This efflux of K(+) from axons results in K(+) accumulation in the interstitial space, causing depolarization of the K(+) reversal potential (E(K)), which can prevent subsequent action potentials. To ensure optimal neuronal function, the K(+) is buffered by astrocytes, an energy-dependent process, which acts as a sink for interstitial K(+), absorbing it at regions of high concentration and distributing it through the syncytium for release in distant regions. Pathological processes in which energy production is compromised, such as anoxia, ischemia, epilepsy and spreading depression, can lead to excessive interstitial K(+) accumulation, disrupting sensitive trans-membrane ion gradients and attenuating neuronal activity. The changes that occur in interstitial [K(+)] resulting from both physiological and pathological processes can be monitored accurately in real time using K(+)-sensitive microelectrodes, an invaluable tool in electrophysiological studies.