Alterations in K+, Ca2+, Na+, and Ba2+ concentrations significantly modulate acetylcholine release from rat motor nerve terminals, highlighting similarities between excitation-transmitter release and excitation-contraction coupling.
These ion-dependent effects on transmitter release warrant no clinical change; leaves open translation to human neuromuscular physiology.
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.
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Elmqvist et al. (1966) studied this question.