Characteristics of activity-dependent potassium accumulation in mammalian peripheral nerve in vitro

Ion-sensitive microelectrodes were used to study the behavior of extracellular ions in rat sciatic nerve during and following activity. Nerve stimulation produced increases in [K+]o that were dependent upon the frequency and duration of stimulation; no change in extracellular pH occurred with stimulation. Increases in [K+]o depended on axonal discharge since they were blocked by inhibiting sodium channels with tetrodotoxin. At 22 degrees C, stimulation could induce increases in [K+]o of several mM; at 36 degrees C, stimulation rarely produced increases in [K+]o greater than 1 mM. Stimulated increases in [K+]o dissipated very slowly (i.e. t 1/2 = 50-100 s) and the rate of dissipation was not significantly affected by anoxia, changes in temperature, changes in extracellular pH, or the application of a blocker of Na+, K(+)-ATPase (ouabain) or a K+ channel blocker (Ba2+). In comparison to the central nervous system, neural activity in rat sciatic nerve produced smaller increases in [K+]o and these increases dissipated much more slowly. The primary mechanism of K+ dissipation appeared to be diffusion, probably facilitated by the larger extracellular space in peripheral nerve compared to the central nervous system, but impeded by diffusion barriers imposed by the blood-nerve barrier.