Characteristics of activity-dependent potassium accumulation in mammalian
peripheral nerve in vitro.
Hoppe D, Chvatal A, Kettenmann H, Orkand RK, Ransom BR
Department for Neurobiology, University of Heidelberg, F.R.G.
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.
