Differential effects of diltiazem on glutamate potentials and excitatory junctional potentials at the crayfish neuromuscular junction.

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Abstract
The effects of diltiazem on glutamate potentials and excitatory junctional potentials (ejps) were investigated in the crayfish neuromuscular junction. 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 ejps elicited by a train of pulses of 100/s increased by about 2 times. Diltiazem might be 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 delayed by diltiazem. The increase in amplitude of ejps caused by diltiazem was due to the increase in membrane resistance. The quantum content and size of extracellular ejps were not affected by diltiazem. The microelectrode technique substantiated that the glutamate sensitive area coincided with the neuromuscular junctional area. The pharmacological difference between glutamate potentials and ejps revealed is difficult to explain on the glutamate transmitter hypothesis. One explanation considered is that there are 2 pharmacologically different kinds of receptors sensitive to L-glutamate.