The effects of tryptamine on transmitter release at a lobster neuromuscular junction

Electrophysiological techniques were employed to characterize the effects of tryptamine at excitatory and inhibitory neuromuscular junctions of the stretcher muscle in the carpopodite of lobster walking limbs. Tryptamine was found to have a concentration dependent, biphasic effect on excitatory junction potential (EJP) amplitude. At concentrations of 0.01-0.5 mM tryptamine increased the amplitude of evoked EJPs, but at higher concentrations (greater than 0.5 mM) the amplitude was decreased by this amine. The high concentrations also decreased the amplitude of inhibitory junction potentials (IJPs) and reduced the frequency of miniature excitatory junction potentials (MEJPs). When a preparation in which the EJPs had been depressed by tryptamine was washed with the control, artificial sea water solution, the EJPs were increased to an amplitude greater than that of the pre-tryptamine control. Current-voltage relationship studies showed that tryptamine did not affect the effective resistance of the muscle fiber membrane. Tryptamine had no effect on the amplitude of excitatory responses evoked by the iontophoretic application of glutamate. Concentrations of tryptamine ranging to 10.0 mM affected neither the conduction velocity in meropodite or that of giant central nervous system (CNS) axons. We conclude that tryptamine affects synaptic transmission pre-synaptically by influencing the transmitter release process. Mass spectrometric analysis showed tryptamine to be an endogenous substance in the lobster; but the concentrations were low in the tissues analyzed. The highest concentration (approximately 0.3 nmol/g wet tissue) was in the subesophageal ganglion. Tryptamine was not detected in the meropodite nerves or carpopodite muscles.