Two-thirds of the tested subesophageal ganglion cells of Japanese snail, Euhadra peliomphala, was hyperpolarized when they were perfused by high K-Ringer. This hyperpolarization was accompanied with a marked decrease in membrane resistance and was independent of cell types classified by ACh-induced response. Pentobarbital was found to convert high K-induced hyperpolarization into depolarization, or to augment K-depolarization. The high K-induced hyperpolarization was considered as the result of summated IPSP's elicited by the presynaptic inhibitory fibers which were primarily depolarized by high K. Pentobarbital may remove this synaptic inhibition and disclose the original K-depolarization underlying the cell. In Cl-free media, high K caused a marked depolarization instead of hyperpolarization, or augmented the depolarization observed in normal Ringer. This suggested that the subsynaptic membrane became permeable to Cl ions during the inhibitory presynaptic activity when high K was applied. ACh was found not to be responsible for this synaptic inhibition, because d-tubocurarine, which is known to block the Cl-dependent ACh response of the snail neurons, did not affect the high K-induced hyperpolarization. The possibility of indirect action of high K on the membrane potential through synaptically mediated inhibition was discussed as a cause of its hyperpolarizing effect.