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.

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Taste receptor cells contain a heterogeneous array of voltage-dependent ion conductances that are essential components for the transduction of gustatory stimuli. Although mechanistic roles have been proposed for several cationic conductances, the understanding of anionic currents is rudimentary. This study characterizes biophysical and pharmacological properties of chloride currents in rat posterior taste cells using whole cell patch-clamp recording technique. Taste cells express a heterogeneous array of chloride currents that displayed strong outward rectification, contained both calcium-dependent and calcium-independent components, and achieved a maximal conductance of almost 1 nS. Reversal potentials altered predictably with changes in chloride concentration. Currents were sensitive to inhibition by the chloride channel pharmacological agents DIDS, SITS, and niflumic acid but were insensitive to 9-AC. Adrenergic enhancement of chloride currents, present in other cell types, was tested on taste cells with the beta-adrenergic agonist isoproterenol (ISP). ISP enhanced the outwardly rectifying portion of the chloride current. This enhancement was calcium dependent and was blocked by the beta-adrenergic antagonist propranolol. Collectively these observations suggest that chloride currents may participate not only in usually ascribed functions such as stabilization of the membrane potential and volume regulation but additionally play active modulatory roles in the transduction of gustatory stimuli.