Influence of Ionic Environment on Acetylcholine Release from the Motor Nerve Terminals

Abstract

Abstract Acetylcholine release from motor nerve terminals in rat diaphragm was estimated as the frequency of miniature end‐plate potentials (m.e.p.p.s). K + 20 mM induced sustained rapid release of m.e.p.p.s which was slow in onset. With higher K + concentration m.e.p.p. frequency rose rapidly. Very high release rates induced by 40 and 50 mM K + were not maintained but declined to a lower sustained level. Augmented m.e.p.p. release could be inhibited by increasing the Ca 2+ concentration above normal. Reduction was approximately 80% with 16 mM Ca 2+ . Reduction of Na + to 1/3 doubled the m.e.p.p. rate. Increase in Ca 2+ raised the rate further in 5 mM K + but reduced it in 20 mM K + . The mechanism of low sodium augmentation of release is obscure but may involve inverse interaction with calcium at an early step in ACh release. Elevation of Ba 2+ to 16 mM gave a transient decline in m.e.p.p. frequency augmented to high level with 20 mM K + , presumably by displacing residual bound calcium. It did not reduce the frequency when Ba 2+ had replaced Ca 2+ in the bathing solution for longer periods. The effects of calcium are discussed and the similarities between excitation‐transmitter release and excitation‐contraction coupling are pointed out.