Glutamate and N-methyl-D-aspartate affect release from crayfish axon terminals in a voltage-dependent manner.

Abstract

In the crayfish neuromuscular junction, the excitatory transmitter is glutamate. The present study shows that at concentrations as low as 5 x 10(-7) M, glutamate affects the depolarization-evoked release of neurotransmitter. Furthermore, the effect of glutamate on release is voltage-dependent and depends on the level of the depolarizing pulse. Nerve terminals were exposed to 5 x 10(-7) M tetrodotoxin and then depolarized to different levels by a macropatch electrode. Depending on the amplitude of the depolarizing pulse, glutamate (5 x 10(-7) to 1 x 10(-5) M) had a dual effect on release. At small depolarizing pulses, glutamate reduced release, whereas at large depolarizing pulses, it enhanced it. Glutamate at 10(-6) M had no significant effect on action-potential-induced release. At 10(-4) M glutamate, the action-potential-induced release was always inhibited. N-Methyl-D-aspartate was found to mimic one of the effects of glutamate: N-methyl-D-aspartate (10(-7) to 10(-5) M) reduced release at small depolarizing pulses but had no effect with larger depolarizations. 2-Amino-5-phosphonovaleric acid blocked the effect of N-methyl-D-aspartate.