The effects of exogenous nitric oxide on the function of neuromuscular synapses.

Extracellular recording experiments using neuromuscular skin/chest muscle preparations from lake frogs were performed at low extracellular Ca2+ ion concentrations to study the effect of L-arginine (the substrate for nitric oxide synthesis) and N(G)-nitro-L-arginine methyl ester (a blocker of NO synthase) on the parameters of evoked transmitter secretion and ion currents in motor nerve endings. L-arginine at a concentration of 100 microM decreased the amplitude of endplate currents as well as their quantum composition, and also increased the amplitude of the third phase of the evoked nerve ending response, which reflects the kinetics of potassium influx currents. N(G)-nitro-L-arginine methyl ester at a condition of 100 microM led to increases in the amplitude and quantum composition of endplate currents and decreased the amplitude of the third phase of the evoked nerve ending response.

Effect of exogenous nitric oxide on electrogenesis in myelinated and unmyelinated nerve fibers.

Extracellular recording was used to study the effect of sodium nitroprusside, a donor of NO, on parameters of action potential and ionic currents in single sciatic nerve fibers and unmyelinated nerve terminals in the sternal muscle in frogs. Sodium nitroprusside significantly decreased the duration of action potential in Ranvier node and the amplitude of afterdepolarization. In motor nerve terminals bathed in low Ca(2+) saline, sodium nitroprusside increased phase III amplitude of the nerve terminal response corresponding to outward potassium currents.

[Effect of endogenous nitric oxide on the nerve-muscle synapse function].

The nitric oxide (NO) precursor L-arginine was found to decrease the amplitude and the quantum content of the EPPs and to increase the amplitude of the AP third deflection in the frog neuromuscular junction of the m. cutaneous pectoris preparation. Inhibitor of the NO synthase NG-nitro-L-arginine methylester exerted opposite effects.

The effects of sodium nitroprusside on mediator release and the functional properties of postsynaptic membranes in the neuromuscular synapse.

Experiments on neuromuscular preparations of frog skin- thoracic muscle and sartorius muscle, using extracellular recording and two-electrode clamping of the muscle fiber membrane potential, were used to study the effects of the nitric oxide donor sodium nitroprusside on endplate currents. At a concentration of 100 microM, sodium nitroprusside sharply decreased the amplitude and quantum composition of the endplate currents, and also decreased the miniature endplate current frequency. The amplitude-time characteristics of miniature endplate currents, the voltage-dependent amplitude, and the decay time constant of miniature endplate currents did not change as compared with controls.

[Effect of sodium nitroprusside on the mediator release and functional properties of the postsynaptic membrane at the neuromuscular junction].

The effect of nitric oxide donor sodium nitroprusside on the end-plate currents was studied under two-electrode voltage-clamp condition at frog neuro-muscular junction. Sodium nitroprusside (10(-4) M) reduced to the half the amplitude of end-plate currents while did not change miniature end-plate currents indicating the presynaptic nature of end-plate depression. In keeping with such suggestion sodium nitroprusside essentially (to 33%) suppressed the frequency of miniature end-plate currents but did not affect the decay time constant and voltage-dependence of miniature end-plate decay.