Effects of barium on cat spinal motoneurons studied by voltage clamp

Abstract

The effects of intra- and extracellularly iontophoresed Ba2+ on outward and inward ionic currents of cat lumbar motoneurons were examined using the technique of somatic voltage clamp. Intracellularly iontophoresed Ba2+ rapidly and reversibly depressed the outward potassium currents (IK) of motoneurons without affecting the leak conductance. The fast-activated potassium current component (IKf) appears to be predominantly affected. Extracellularly iontophoresed Ba2+ results in the appearance of a persistent inward barium current (IBa) when the membrane potential is depolarized. In addition, IKf is depressed, and extracellular Ba2+ must enter the cell to exert at least part of its IK-blocking action. Leak conductance (GL) is usually decreased also. The voltage dependence of IBa is similar to that of the natural persistent inward current, Ii, but IBa can develop even when Ii has disappeared due to impalement injury. IBa is also seen in cells in which all Na current appears to have been blocked by intracellular injection of the lidocaine derivative, QX314 [N-(2,6-dimethylphenyl)carbamoylmethyltriethylammonium bromide]. IBa enters through Ca2+-conductance channels that normally carry Ii. These channels must remain present even though Ii usually deteriorates after impalement. Other properties of IBa were investigated. IBa is non- or slowly inactivating over a large voltage range. IBa onset and decay appeared to be rapid at every potential where IBa is visible. The slowly activated IK component (IKs) is mixed with IBa, even when IBa is large and net inward. Although Ba2+ iontophoresis depresses IKf, the motoneuron action potential shows only a relatively small increase in duration when the net ionic current (IBa + IK + IL) is outward. A prolonged Ba spike occurs only when the net current is inward. Based on these and previous results, a qualitative test for the presence of an Ii-like current in mammalian neurons is proposed. Greatly enhanced spontaneous and evoked excitatory postsynaptic potentials occurred transiently after extracellular Ba2+ iontophoresis, suggesting that Ba2+ enhances release of transmitter in the mammalian spinal cord by its action on presynaptic terminals or axons. The present data support several previous conclusions about the properties of Ii, including the inference that it is generated on or near the soma.