Internal cesium ions block various K conductances in spinal motoneurons.

Conventional intracellular recording with low resistance electrodes was used to examine the effects of iontophoretic injections of Cs+ ions (30-200 nA for 30-500 s) into spinal motoneurons of cats anesthetized with pentobarbital and paralyzed with gallamine. The most striking effects of internal Cs+ were a great prolongation of the falling phase of action potentials, a large reduction in the amplitude of their afterhyperpolarizations, and a considerable increase in the size of delayed depolarizations. A reduction of resting membrane conductance (up to half of control values) and a small increase in membrane potential usually were evident. Although the rate of rise and amplitude of spikes sometimes were increased, the above effects on membrane properties usually were accompanied by block of antidromic invasion or synaptic spike generation, and inactivation of directly evoked spikes. Recovery of spike genesis was very rapid but the prolongation of spikes and other effects of Cs+ lasted 4-35 min, depending on the amount of Cs+ application. Larger injections of Cs+ resulted in greater depolarizations of up to 13 mV. It is concluded that internal Cs+ ions block voltage-dependent K+ conductance of spike repolarization, the Ca2+-activated K+ conductance responsible for the afterhyperpolarization, and some of the K+ conductance responsible for the resting potential. It is suggested that the enhanced delayed depolarization may result from a Cs+-blockade of an early outward K+ current which would unmask an inward current of Ca2+ ions.