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In the endplates of rat phrenic nerve-diaphragm, application of the acetylcholine-like compound, carbachol, causes a marked increase in transmitter release, as measured electrophysiologically using miniature endplate potential frequency. Washing out of carbachol reverses the increase in frequency. The ability of carbachol to increase transmitter release is greatly enhanced by perfusion of the preparation with Ringer solution containing elevated K(+). At concentrations of carbachol greater than 30 muM, the onset of the postjunctional blocking action of carbachol is too rapid and obscures the increase in miniature potential frequency. The rate of increase in transmitter release is dependent on the concentration of carbachol applied and can be antagonized by d-tubocurarine (10-60 nM) and other blocking compounds. These findings, in contrast to previous reports, indicate that cholinergic nerve endings, like adrenergic nerve endings, respond to applied acetylcholine-like drugs with measurable increases in transmitter output.

1 In the perfused superior cervical ganglion of the cat manganese ions (2.7 - 4.6 mM) caused a block of synaptic transmission and reduced the output of acetylcholine.2 Calcium ions (8.4-10.5 mM) relieved the synaptic block produced by manganese and partially restored the acetylcholine output.3 The presence of manganese also reduced the sensitivity of ganglion cells to injected acetylcholine.4 Both effects of manganese were completely reversible.