Postsynaptic effects of nickel ions at the insect neuromuscular junction.

The effect of extracellular nickel on the excitatory postsynaptic response at the insect neuromuscular junction was studied in the segmental muscle of the larval mealworm Tenebrio molitor. The response to L-glutamate applied iontophoretically (glutamate potential, GP) was potentiated in the presence of Ni2+ though the excitatory postsynaptic potential (EPSP) was reduced. It seems unlikely that Ni2+ acts at the same binding site as L-glutamate does since the value of the limiting slope of double logarithmic plots for the action of glutamate was increased in the presence of Ni2+. The potentiation of GP in the presence of Ni2+ cannot be ascribed to competition between Ni2+ and Ca2+ since GP amplitude did not show any dependence on the concentration of Ca2+. Nickel ions did not alter the reversal potential of excitatory postsynaptic current (EPSC) and glutamate current (GC) under the voltage clamp condition, whereas the amplitude of GC was potentiated in the presence of Ni2+. The time constant of the decay of EPSC showed a weak voltage dependency: the more depolarized the membrane, the more prolonged the time constant. In the presence of 1 mM Ni2+ the amplitude of miniature EPSCs (MEPSCs) increased and the half decay time was prolonged significantly. These results suggest that Ni2+ interacts with charged groups near the glutamate receptor-channel complex so that the kinetics of the channel are altered.