• E M Silinsky.
• Department of Molecular Pharmacology, Northwestern University Medical School, Chicago, IL 60611, USA. e-silinsky@nwu.edu
• Br. J. Pharmacol. 2000 Jan 1;129(2):360-6.

Abstract1. The effects of Ba(2+) (0.1 - 2 mM) on the component of the perineural voltage change associated with nerve terminal calcium currents (prejunctional Ca(2+) currents) were compared with the effects of this ion to antagonize calcium-dependent acetylcholine (ACh) release. These experiments were made on isolated neuromuscular junctions of the frog. 2. In the presence of sufficient concentrations of K(+) channel blockers to eliminate measurable prejunctional K(+) currents, low concentrations of Ba(2+) selectively antagonized prejunctional Ca(2+) currents in normal Ca(2+) solutions. Higher concentrations of Ba(2+) also substantially reduced the Na(+) component of the perineural waveform. 3. Ba(2+) inhibited the prolonged prejunctional Ca(2+) currents that developed in the presence of higher concentrations of K(+) channel blockers. 4. Simultaneous measurements of the prejunctional Ca(2+) currents and the electrophysiological correlates of ACh release (i.e. end-plate potentials, EPPs) were made under conditions of modest K(+) channel blockade. Under these conditions, Ba(2+) generally produced simultaneous decreases in both Ca(2+) currents and EPP amplitudes. In some instances, a prolongation of prejunctional Ca(2+) currents and a transient increase in EPP amplitudes preceded the decreases in both electrophysiological events. 5. These results suggest that Ba(2+) ions can antagonize the entry of calcium into motor nerve endings and this effect is likely to be responsible for the inhibitory effects of Ba(2+) on evoked ACh release.

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