The effects of alkaline cations on the responses of cat spinal motoneurons, and their removal from the cells

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Abstract
Potassium, rubidium, caesium and lithium ions were electrophoretically injected into cat spinal motoneurons. The rising slope of the spike potential was slowed by lithium as well as sodium ions, but not by potassium, rubidium or caesium ions. The falling slope of the spike potential and the after-hyperpolarization following the spike were changed by lithium and caesium as well as by sodium ions, but not by potassium or rubidium ions. It is postulated that lithium ions pass through the sodium channels in the active membrane, and rubidium ions through the potassium channels, but caesium ions through neither. Injections of any alkaline cations change the inhibitory postsynaptic potential in the depolarizing direction. This is explained by assuming that chloride ions move into the cell during the passage of cation-injecting currents. The rates of cation extrusion from motoneurons were estimated from the recovery time courses of the motoneuronal potentials. It is suggested that caesium ions are removed from the cell through the diffusion channels in the resting membrane with a rate comparable to that for sodium extrusion; and that lithium ions are extruded by the sodium pump with about half the rate for sodium extrusion.