The voltage-dependent K + channels of the mammalian sarcolemma were studied with the patchclamp technique in intact, enzymatically dissociated fibres from the toe muscle of the mouse. With a physiological solution (containing 2.5 mM K § in the pipette, depolarizing pulses imposed on a cell-attached membrane patch activated K + channels with a conductance of about 17 pS. No channel activity was observed when the pipette solution contained 2mM tetraethylammonium (TEA), or 2 mM 4-aminopyridine (4-AP). Whole cell recordings from these very small muscle fibres showed the well-known delayed rectifier K + outward current with a threshold of about -40 mY. The whole-cell current was completely blocked by 2 mM TEA in the bath, suggesting that the TEA-sensitive channels in the patch were also delayed rectifier channels. The inactivation properties of the channels were studied in the cell-attached mode. Averaged single-channel traces showed at least two types of channels discernible by their inactivation time course at a test potential of 60 mV. The fast type inactivated with a time constant of about 150ms, the slow type with a time constant of about 400 ms. A little channel activity always remained during pulses lasting several minutes, indicating either the presence of a very slowly inactivating third type of K + channel, or the tendency of the fast inactivating channels to re-open at constant voltage. No difference was seen in the single-channel amplitudes of the different types of K + channels. The well characterized adenosine-5'-triphosphate-(ATP)-sensitive and Ca2+-dependent K + channels, although present, were not active under the conditions used. The results suggest that in mouse skeletal muscle the delayed rectifier channels to not only carry the outward current during excitation but are also responsible for the resting K + conductance.