Control of Extracellular potassium in the mammalian spinal cord

Abstract

Using potassium specific double barreled microelectrodes, the time course of changes in the concentration of K÷ ions in the extracellular space [K÷] e, of the lumbar spinal cord was examined after peripheral tetanic stimulation and after a single volley in a mixed peripheral nerve in non-anaesthetized, intercollicularly decerebrated and spinalized cats. Tetanic stimulation (100 Hz), which increases the [K÷) e from 3 to 9 m M, is followed by a long-lasting phase of reduced [K÷] e during which [K÷] e decreases down to a level 0.5 m M below the resting level and remains there for 1-2 min before returning to its original resting level. The high sensitivity to the oxygen supply of this subnormal phase of [K÷] e reflects its metabolic character in the active processes redistributing the accumulated K÷ ions from extracellular space. The appearance of a subnormal phase of [K÷] e is primarily dependent on the position of the microelectrode in the pool of discharging neurones and not on the absolute level of the increased [K÷] e. This is considered as evidence that the processes responsible for active reabsorption of K÷ ions from the extracellular space are located in the neurones and not in the glial cells. The increased [K÷] e is reflected in locally recorded potentials as a negativity and the decreased [K÷] e as a positivity. The latency of locally recorded positivity is, however, shorter than the latency of reduced [K÷) e and therefore it is likely that it reflects not only passive hyperpolarization of glial elements, but also electrogenic currents passing across the neuronal membrane produced by active ionic transport.