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Effects of prostaglandins (PGs) on the neuromuscular junction of the guinea-pig vas deferens were investigated by the micro-electrode and double sucrose gap methods. 1. PGE1, PGE2 or PGF2 alpha (10(-10) to 10(-7) g/ml.) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential. 2. PGs markedly suppressed the amplitude of excitatory junction potential (e.j.p.) but the facilitation phenomena seen with repetitive stimulation were not affected. PGs did not change the amplitude and frequency of the miniature e.j.p. 3. The action potential recorded from the small nerve bundle with the aid of an extracellular micro-electrode method was not affected by PGS. 4. The amplitude of the e.j.p. was dependent on the external concentration of Ca. When plotted against [Ca]o on a double log scale, the above relation yielded a straight line with a slope of 1.0. Application of PGs resulted in a parallel shift of this relation to the right. 5. From the concentrations of [Ca]o to produce a given e.j.p. in the absence and presence of various concentrations of PGE1, the linear relation was observed from double logarithmic plot between [[Ca]o ratio -1] and [PGE1]o. However the slope of the line was too small (-0.37) to indicate a simple competition between [PGE1]o and [Ca]o. 6. Indomethacin (10(-6) g/ml.) had no effect on the amplitudes of e.j.p. produced by repetitive stimulation. 7. These results indicate that a low concentration of PGs interact with [Ca]o at the activated nerve terminals, but that there is no modification of the actions of Ca in the nerve terminals required for release of chemical transmitter.