The action of (+)-tubocurarine on the extracellular excitatory postsynaptic current (EPSC) and on the L-glutamate-induced current relaxation after voltage jumps was studied at a neuromuscular junction of the meal-worm larva (Tenebrio molitor) where L-glutamate is a candidate transmitter. During hyperpolarizing voltage jumps, the glutamate-induced current relaxed along an exponential time course to a new steady state. The rate constant (α(relax)) for the glutamate current relaxation was slightly increased by hyperpolarization. Potential dependence of α was expressed by α(relax) = a . exp(AV), with a = 0.3073 and A = -0.0050 in a typical fiber exposed to 5 x 10-4 M L-glutamate. (a and A are constants and V is the membrane potential.) α(relax) increased with increasing agonist concentration betwen 5 x 10-5 and 1 x 10-3 M. In the presence of (+)-tubocurarine, the glutamate-induced current relaxed in the direction of decreasing conductance during hyperpolarizing voltage steps in contrast to the normal situation. The rate constant for this 'outward' relaxation was increased by hyperpolarization. (+)-Tubocurarine produced a negative slope in the membrane potential-glutamate current relationship with hyperpolarization. (+)-Tubocurarine (>2 x 10-4 M) dramatically shortened the decay of the extracellular EPSC in a voltage-dependent fashion; hyperpolarization strongly facilitated the decay. It is suggested that the (+)-tubocurarine-induced block of the glutamate synapse results from blocking of open ionic channels at a site lying within the transmembrane electric field.
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