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Neuromuscular transmission in crustaceans is enhanced by a sodium ionophore, monensin, and by prolonged stimulation.
Author(s) -
Atwood H L,
Charlton M P,
Thompson C S
Publication year - 1983
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1983.sp014527
Subject(s) - monensin , ionophore , calcium , chemistry , biophysics , stimulation , excitatory postsynaptic potential , sodium , tetrodotoxin , neuromuscular transmission , calcium in biology , neurotransmission , intracellular , endocrinology , biochemistry , biology , receptor , organic chemistry
A sodium ionophore, monensin, was applied to crustacean neuromuscular preparations to determine whether increased intracellular sodium could lead to enhancement of transmitter release similar to that observed with prolonged stimulation. Following a single application of monensin (3‐13 microM), the excitatory postsynaptic potential (e.p.s.p.) 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 second application of monensin was less effective than the first. Application of monensin in calcium‐free solutions led to rapid, marked enhancement of the e.p.s.p. upon restoration of the normal physiological solution, indicating that monensin can produce its effects in the absence of external calcium. Spontaneous miniature potentials often occurred more frequently in calcium‐free solution after monensin had been applied. The extent of enhancement of e.p.s.p. amplitude depended on the concentration of external sodium, being smaller in solutions of low sodium. Prolonged stimulation of the motor axon usually enhanced the e.p.s.p. to a greater extent than application of monensin alone, but the time course of recovery of e.p.s.p. amplitude was similar in both cases. We conclude that the increase in e.p.s.p. amplitude promoted by monensin can be attributed to increased transmitter output resulting from influx of sodium into the nerve terminal. Increased intracellular sodium may lead to a rise in intracellular calcium ion concentration. Some features of long‐term facilitation of transmitter release can be attributed to build‐up of intracellular sodium during stimulation.