LACK OF VOLTAGE-SENSITIVE POTASSIUM CHANNELS AND GENERATION OF MEMBRANE-POTENTIAL BY SODIUM-POTASSIUM ATPASE IN MURINE T-LYMPHOCYTES

Voltage sensitive K+ channels, which are responsible for generation of membrane potential in most cells, are functionally absent in about on e-third of peripheral murine T cells and greatly reduced in the rest a s shown by resistance of their membrane potential to changes in extrac ellular potassium concentration and failure of K+ channel dependent vo lume regulation. Despite the absence of voltage- sensitive K+ channels , the membrane potential of peripheral T cells is between -60 and -70 mV, the same as thymocytes. A total of 40 to 70 mV of the membrane pot ential of peripheral T cells is produced by the direct electrogenic ac tion of the asymmetric Na+K+ ATPase pump because the cells are depolar ized by ouabain, an inhibitor of the pump, removal of extracellular po tassium or reduction of temperature. The residual, ouabain-resistant m embrane potential, is sensitive to the K+ channel blocker, quinine, an d thus due to electrodiffusion through K+ channels. Na+ and K+ turnove r, and sensitivity to ouabain, are the same in peripheral T cells and thymocytes. The predominant mechanism of membrane potential generation changes during T lymphocyte differentiation from electrodiffusion in the thymus to electrogenic in peripheral T cells and back to electrodi ffusion upon peripheral cell activation.