Extracellular potassium concentration, [K(+)](o), and intracellular calcium, [Ca(2+)](i), rise during neuron excitation, seizures
and spreading depression. Astrocytes probably restrain the rise of K(+) in a way that is only partly understood. To examine
the effect of glial K(+) uptake, we used a model neuron equipped with Na(+), K(+), Ca(2+) and Cl(-) conductances, ion pumps
and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either "passive", incorporating only
leak channels and an ion exchange pump, or it had rectifying K(+) channels. We computed ion fluxes, concentration changes
and osmotic volume changes. Increase of [K(+)](o) stimulated the glial uptake by the glial 3Na/2K ion pump. The [K(+)](o)
flux through glial leak and rectifier channels was outward as long as the driving potential was outwardly directed, but it
turned inward when rising [K(+)](o)/[K(+)](i) ratio reversed the driving potential. Adjustments of glial membrane parameters
influenced the neuronal firing patterns, the length of paroxysmal afterdischarge and the ignition point of spreading depression.
We conclude that voltage gated K(+) currents can boost the effectiveness of the glial "potassium buffer" and that this buffer
function is important even at moderate or low levels of excitation, but especially so in pathological states.