1) The effect of dimorpholamine (DMA) 1.5×10
-4g/ml on the neuromuscular junction was studied in the abductor muscle of crayfish walking leg. Excitatory and inhibitory junctional potentials (e. j. p. s. and i. j. p. s.) were induced by a train of 6-8 successive stimuli at a rate of 80-100/sec and were recorded by an intracellular or extracellular electrode.
2) DMA increa s ed the amplitude of intracellularly recorded e. j. p. to 2-4 times the control size. DMA augmented the degree of facilitation of e. j. p. s.
3) DMA increased the input resistance of a muscle fiber by 20-60 %.
4) DMA increased the am plitude of extracellular e. j. p. s. The probability of neuromuscular failure,
i. e. the failure of the nerve impulse to set up an extracellular e. j. p., was reduced by DMA.
5) DMA did not produce any remarkable change either in the size of extracellularly recorded spontaneous miniature e. j. p. s, or in the quantum size of extracellular e. j. p. s produced by a repetitive stimulation.
6) The main mechanism of action of DMA to increase the size of e. j. p. is an increase in the amount of excitatory transmitter released from the terminals by nerve impulses. A second mechanism of action of DMA is an increase in membrane resistance of the muscle fiber.
7) Under the action of DMA the amplitude of intracellular i. j. p. was increased by a factor of 1.2-3, while the sensitivity to γ-aminobutyric acid of the postsynaptic membrane did not show any conspicuous change.
8) The main mechanism of action of DMA to augment the i. j. p. size is the increase in membrane resistance of the muscle fiber. It is suggested that the increased output of the inhibitory transmitter from nerve terminals is also involved in the mechanism of action.
9) The possibility th at DMA may affect non-cholinergic synapses in mammalian central nervous system was discussed.
抄録全体を表示