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1. The effects of diltiazem on glutamate potentials and excitatory junctional potentials (e.j.p.s) were investigated in the crayfish neuromuscular junction. 2. When diltiazem (0.3 mM) was added to the perfusion fluid, the ionophoretic glutamate potential was reduced to about half, whereas the peak amplitude of successive e.j.p.s elicited by a train of pulses of 100/sec increased by about 2 times. 3. It was suggested that diltiazem was a non-competitive inhibitor of L-glutamate. The reduction of the response to applied glutamate was not due to the acceleration of desensitization of the glutamate receptor. The rate of recovery from desensitization was delayzed by diltiazem. 4. The increase in amplitude of e.j.p.s caused by diltiazem was due to the increase in membrane resistance. The quantum content and size of extracellular e.j.p.s were not affected by diltiazem. 5. It was substantiated using the micro-electrode technique that the glutamate sensitive area coincided with the neuromuscular junctional area. 6. The pharmacological difference between glutamate potentials and e.j.p.s revealed in the present study is difficult to explain on the glutamate transmitter hypothesis. One explanation worthy to be considered is that there are two pharmacologically different kinds of receptors sensitive to L-glutamate.