The extrusion of sodium from cat spinal motoneurons

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Abstract
Sodium ions were injected into cat spinal motoneurons electrophoretically through an intracellular NaCl-filled microelectrode. Following an injection there were characteristic changes in the resting and spike potentials, the after-potential and the inhibitory postsynaptic potential, all of which recovered within about 7 min. The maximum rising slope of the spike recovered exponentially, suggesting the exponential decrease of the intracellular sodium concentration by the operation of the sodium pump in actively extruding excess sodium. The time course of the recovery of the maximum falling slope of the spike paralleled that of the rising slope, indicating a reciprocal change in the intracellular sodium and potassium concentrations. There was a good parallelism in the time courses of the recovery of the amplitude of the after-potential and the maximum falling slope of the spike, as would be expected from their postulated dependence on the same internal potassium concentration. The inhibitory postsynaptic potential recovered from its displacement in the depolarizing direction with the same time course as did the other potentials, which indicates parallel decreases of the intracellular sodium and chloride concentrations. From the exponential recovery curves obtained for these potentials, the rate constant of active sodium extrusion was estimated as 40 h$^{-1}$. The fast rate of sodium extrusion in cat motoneurons is related to the dynamic ionic balance in neurons of the central nervous system, and is explained by the geometry and by the membrane properties of motoneurons.