This article reviews some recent studies on the voltage-gated ion channels in the plasmalemma of the satellite cells of the peripheral and central nervous systems. Following the finding that rabbit Schwann cells exhibit a large binding capacity for saxitoxin (Ritchie and Rang, 1983) electrophysiological studies have shown that these cells not only express plasmalemmal voltage-gated sodium channels but also voltage-gated potassium channels (Chiu, Shrager and Ritchie, 1984; Shrager, Chiu and Ritchie, 1985). Whole-cell recording with the patch-clamp method reveals that the properties of these two kinds of channel are quite similar to those of the corresponding channels in the nodal axolemma, except that the peak current-voltage relation of the sodium channels is shifted about 30 mV in the depolarizing direction. Similar voltage-gated sodium and potassium channels exist in rat cultured astrocytes (Bevan et al., 1985). Furthermore, the outward current on depolarization in astrocytes has a component other than that carried in the potassium channels. About 75% of the total outward current is blocked by external TEA or internal caesium; and it is presumed to be a potassium current. The remainder, however, is insensitive to these potassium channel blocking agents; but it is abolished by exposure to the two stilbene sulphonates, DIDS and SITS (Gray and Ritchie, 1986). This remaining current persists in the presence of the large organic cation N-methyl-(+)-glucamine in the patch pipette. It is, however, reduced when the chloride of the external medium is replaced by methyl-sulphate, sulphate, or isethionate; and it is abolished when the external anion is gluconate (MW, 190). The TEA-insensitive component of outward current in astrocytes thus seem to involve an influx of chloride ions through a voltage-gated channel whose diameter is such that anions larger than gluconate cannot pass. The current in the channels is neglible at potentials more negative than about-40 mV.