Trimethaphan as a glutamate inhibitor at the crayfish neuromuscular junction.
At the crayfish neuromuscular junction trimethaphan reduced the amplitude of both the glutamate-induced synaptic current and the excitatory junctional current in a dose-dependent manner at concentrations greater than 5 microM. These effects were dependent on membrane potential. Trimethaphan did not affect the inhibitory junctional potential and the input resistance of the opener muscle. The dose-response curves for inhibition of glutamate responses by trimethaphan suggest that trimethaphan is not a competitive glutamate antagonist. A quantum analysis of extracellularly recorded excitatory junctional potentials showed that trimethaphan decreased both quantum content and average unit size. Trimethaphan also prolonged the glutamate currents evoked by both short and prolonged ionophoretic currents, but the decay of nerve-evoked synaptic currents was accelerated by the drug. Three explanations worthy of consideration to explain the action of trimethaphan are the responses of extra-junctional receptors, the sudden release and short actions of the neurotransmitter in contrast with the progressive application and long exposure of exogenous agonists to receptors, and discrimination of glutamate and excitatory transmitter in the crayfish neuromuscular junction. The second of these possibilities is mainly discussed at length.
D000818:Animals; D003400:Astacoidea; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D014294:Trimethaphan / Q000494:pharmacology*
D005971:Glutamates; D018698:Glutamic Acid; D014294:Trimethaphan