[Presynaptic action of armin and galantamin on mammalian neuromuscular junction].

Actions of the two cholinesterase inhibitors: armin and galanthaamine on the neuromuscular transmission and on the spontaneous and evoked acetylcholine release were studied in the rat diaphragm. High concentrations (greater than or equal to 10(-6) g/ml) of these agents exhausted the available transmitter store which decreased the quantum content of e. p. p. sin single nerve stimulation. At the repetitive stimulation (10-100 s-1), armin and galanthaamine accelerated the presynaptic depression of e. p. p. s and slowed down the rate of transmitter mobilization. This resulted in a rapid decrease of quantum content and amplitude of e. p. p. s. The found presynaptic deteriorations together with the stationary postsynaptic depolarization may cause the neuromuscular block.