Neuromuscular transmission in crustaceans is enhanced by a sodium ionophore, monensin, and by prolonged stimulation.

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Abstract
A sodium ionophore, monensin, was applied to crustacean [Libinia emarginata, Homarus americanus and Ovalipes] neuromuscular preparations to determine whether increased intracellular Na could lead to enhancement of transmitter release similar to that observed with prolonged stimulation. Following a single application of monensin (3-13 .mu.M), the excitatory postsynaptic potential (EPSP) increased in amplitude by 50-800%. The increase was entirely due to a presynaptic effect that resulted in higher quantal content of transmission and increased frequency of spontaneous miniature potentials. A 2nd application of monensin was less effective than the first. The extent of enhancement of EPSP amplitude depended on the concentration of external sodium, being smaller in solutions of low sodium. Prolonged stimulation of the motor axon usually enhanced the EPSP to a greater extent than application of monensin alone, but the time course of recovery of EPSP amplitude was similar in both cases. The increase in EPSP amplitude promoted by monensin can be attributed to increased transmitter output resulting from influx of Na into the nerve terminal. Increased intracellular Na may lead to a rise in intracellular Ca ion concentration. Some features of long-term facilitation of transmitter release can be attributed to build-up of intracellular Na during stimulation.