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. It is suggested that endogenous nitric oxide is produced in frog neuromuscular synapses, which in normal conditions suppresses transmitter secretion and modulates the function of potassium channels in the nerve ending.