Article date: January 2000
By: Eugene M Silinsky, in Volume 129, Issue 2, pages 360-366
The effects of Ba2+ (0.1–2 mM) on the component of the perineural voltage change associated with nerve terminal calcium currents (prejunctional Ca2+ 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.
In the presence of sufficient concentrations of K+ channel blockers to eliminate measurable prejunctional K+ currents, low concentrations of Ba2+ selectively antagonized prejunctional Ca2+ currents in normal Ca2+ solutions. Higher concentrations of Ba2+ also substantially reduced the Na+ component of the perineural waveform.
Ba2+ inhibited the prolonged prejunctional Ca2+ currents that developed in the presence of higher concentrations of K+ channel blockers.
Simultaneous measurements of the prejunctional Ca2+ 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, Ba2+ generally produced simultaneous decreases in both Ca2+ currents and EPP amplitudes. In some instances, a prolongation of prejunctional Ca2+ currents and a transient increase in EPP amplitudes preceded the decreases in both electrophysiological events.
These results suggest that Ba2+ ions can antagonize the entry of calcium into motor nerve endings and this effect is likely to be responsible for the inhibitory effects of Ba2+ on evoked ACh release.
The effects of Ba2+ (0.1–2 mM) on the component of the perineural voltage change associated with nerve terminal calcium currents (prejunctional Ca2+ 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.
In the presence of sufficient concentrations of K+ channel blockers to eliminate measurable prejunctional K+ currents, low concentrations of Ba2+ selectively antagonized prejunctional Ca2+ currents in normal Ca2+ solutions. Higher concentrations of Ba2+ also substantially reduced the Na+ component of the perineural waveform.
Ba2+ inhibited the prolonged prejunctional Ca2+ currents that developed in the presence of higher concentrations of K+ channel blockers.
Simultaneous measurements of the prejunctional Ca2+ 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, Ba2+ generally produced simultaneous decreases in both Ca2+ currents and EPP amplitudes. In some instances, a prolongation of prejunctional Ca2+ currents and a transient increase in EPP amplitudes preceded the decreases in both electrophysiological events.
These results suggest that Ba2+ ions can antagonize the entry of calcium into motor nerve endings and this effect is likely to be responsible for the inhibitory effects of Ba2+ on evoked ACh release.
British Journal of Pharmacology (2000) 129, 360–366; doi:10.1038/sj.bjp.0703036
DOI: 10.1038/sj.bjp.0703036
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