Abstract
Following a previous paper two methods were employed in a further investigation of the sodium pump in cat spinal motoneurons: (1) to compare the rate of sodium extrusion at different levels of the resting potential, and (2) to depress the sodium pump by the electrophoretic injection of metabolic inhibitors into the cells. The rate of sodium extrusion was found to be independent of the resting potential level, which suggests that the diffusion channels were not a main route for the sodium extrusion. A successful temporary block of the sodium pump was made by the intracellular injection of azide ions.