The nature and origin of calcium‐insensitive miniature end‐plate potentials at rodent neuromuscular junctions.

Abstract

1. To study the nature and origin of slow‐rising, Ca2+‐insensitive miniature end‐plate potentials (m.e.p.p.s) in mammalian muscle we used intracellular recording techniques and drugs which block acetylcholine (ACh) synthesis or the uptake of ACh into synaptic vesicles. Slow m.e.p.p.s were induced in vivo by paralysing the extensor digitorum longus muscle of the rat with botulinum toxin type A or in vitro by the application of 4‐aminoquinoline to the mouse diaphragm nerve‐muscle preparation. 2. Hemicholinium‐3, which blocks ACh synthesis, reduced the amplitude of all synaptic potentials including slow m.e.p.p.s, but only if the nerve was stimulated. 3. 2(4‐phenylpiperidino)cyclohexanol (AH‐5183), which blocks the active uptake of ACh into synaptic vesicles, reduced both the frequency and the amplitude of slow m.e.p.p.s and did so without requiring nerve stimulation. 4. No correlation was observed between the molecular leakage of ACh from the motor nerve and the frequency and amplitude of slow m.e.p.p.s. 5. We conclude that slow m.e.p.p.s are caused by the release of ACh from the nerve terminal, possibly from a small pool of synaptic vesicle‐like structures. © 1986 The Physiological Society