Glutamate inhibitors in the crayfish neuromuscular junction

1. The effects of chlorisondamine and TI-233 on the crayfish neuromuscular junction were investigated in order to compare the action of glutamate with that of the excitatory transmitter. 2. The glutamate-induced synaptic current was inhibited by both of these two drugs. Excitatory junctional potentials were significantly reduced by chlorisondamine, whereas they were increased by TI-233. 3. It is suggested that chlorisondamine and TI-233 are powerful non-competitive antagonists for glutamate. 4. A quantum analysis of extracellular EJPs demonstrated that chlorisondamine did not possess presynaptic action in the crayfish neuromuscular junction. Chlorisondamine shortened the decay phase of extracellular EJPs, and the decay was frequently fitted by a double exponential in relatively low concentrations. 5. Semilogarithmic plots of the decay phase of the glutamate current evoked by a short glutamate pulse were nearly linear, but they shifted from linearity to some extent in the presence of chlorisondamine, showing prolongation of the glutamate current tails. 6. When TI-233 was added to the bathing solution at a concentration of 0.1 mM, the quantum content of extracellular EJPs was increased by about two times, but the average unit size was not changed. 7. There was no change in the rise time and the decay phase of the glutamate potential in the presence of TI-233. 8. Pharmacological difference between glutamate responses and EJPs was revealed in the presence of chlorisondamine and TI-233. Unless this difference can be explicated with a reasonable explanation on the glutamate transmitter hypothesis, it is difficult to confirm that glutamic acid is an excitatory transmitter at the crayfish neuromuscular junction.