Voltage-dependent sodium currents were analyzed in detail from dissociated mammalian taste receptor cells using the whole-cell patch clamp technique. Approximately 50-75% of all taste receptor cells expressed sodium currents. These currents activated close to -50 mV (holding potential = -80 mV) with maximal currents most often occurring at -10 mV. The distribution of maximal inward currents across all cells appeared to display two peaks, at -254 pA and -477 pA, possibly due to differences in sodium channel density. Inward currents were eliminated by replacing 90% of external sodium with N-methyl-D-l-glucamine. The current-voltage relationship of the activated current, as measured by a tail current analysis, was linear, suggesting an ohmic nature of the open channel conductance. The relationship between the time to the peak activated current and the step potential was well fit by a double exponential curve (tau1 = 6.18, tau2 = 37.8 msec). Development of inactivation of the sodium current was dependent upon both voltage- and temporal-parameters. The voltage dependence of the time constant (tau) obtained from removal of inactivation, development of inactivation, and decay of the sodium current displayed a bell-shaped curve with a maximum of 55 msec at -70 mV. In addition to fast inactivation (half maximal at -50 mV), these currents also displayed a slow inactivation (half maximal at -65 mV). Voltage-dependent sodium currents were reversibly inhibited by nanomolar concentrations of tetrodotoxin (Kd = 10(-8) M). There was no evidence of a TTX-insensitive sodium current. This description broadens our understanding of gustatory transduction mechanisms with a particular relevance to the physiological role of receptor cell action potentials.