A function of delayed rectifier potassium channels in glial cells: maintenance of an auxiliary membrane potential under pathological conditions

Muller glial cells from human and guinea-pig retinae were investigated usin g the whole-cell patch-clamp technique. Human Muller cells from eyes with d ifferent diseases were characterized by diminished inwardly-rectifying K+ c urrents. A comparable reduction of these currents was achieved in guinea pi g Muller cells by treatment with iodoacetate to generate ischemia-like cond itions. Consequently, the membrane potentials were reduced significantly in both diseased human and iodoacetate-treated guinea-pig Muller cells as com pared to normal controls. However, the potentials were still clearly negati ve. Delayed rectifier currents could still be recorded under these conditio ns. Application of quinine blocked the delayed rectifier K+ channels, and r esulted in a total breakdown of the membrane potentials. Thus, it becomes a pparent that the glial delayed rectifier K+ channels are necessary to maint ain an 'auxiliary' membrane potential under certain pathological conditions that are characterized by an almost total loss of inward rectifier conduct ance. Therefore, the delayed rectifier K+ channels of glial cells may becom e crucial for the support of basic glial functions. (C) 2000 Elsevier Scien ce B.V. All rights reserved.