Effect of elevated potassium ion concentrations on electrically evoked release of [ 3H]acetylcholine in slices of rat hippocampus

Abstract

To establish the effect of raising the concentration of extracellular potassium ions on axonal conduction and transmitter release in a mammalian central pathway, the septohippocampal cholinergic tract, the rate of [ 3H]acetylcholine release evoked by electrical stimulation was measured in rat hippocampal slices superfused with Krebs' solution containing 3–15 m m K +. The evoked release of [ 3H]acetylcholine was abolished by the presence of tetrodotoxin or by the omission of Ca 2+ in the superfusion medium, indicating that it originated from terminals depolarized by conducted action potentials. Potassium concentrations between 3 and 8m m had no effect but 10–15 m m K + reduced the rate of evoked release and decreased the size of the releasable pool of [ 3H]acetylcholine. Decreasing the sodium content of the Krebs' solution to 97 m m or less had effects similar to those of elevated [K +]. Elevated K + (10–15 m m) reversibly reduced the size of compound action potentials in the fimbria and the alveus. The results suggest that extracellular potassium concentrations occurring under physiological conditions do not affect axonal conduction and transmitter release but that both are reduced in pathological states when extracellular [K +] above 8 m m occur.