How taste receptor cells participate in encoding disparate compounds into distinct taste qualities represents a fundamental problem in the study of gustatory transduction mechanisms. Quinine is the most common stimulus employed to represent bitterness yet its electrophysiological consequences on voltage-dependent ion channels in the taste receptor cell have not been elucidated in detail. This study examines such effects on taste receptor cells dissociated from the foliate and circumvallate papillae of the rat. Outward potassium currents, which include transient, sustained and calcium-activated components, were reversibly inhibited by bath application of quinine, with an IC50 of 5.1 x 10(-6) M. The time course of the current traces, along with voltage shifts in normalized conductance and inactivation curves, suggests that multiple mechanisms of inhibition may be occurring. Inwardly rectifying potassium currents were unaffected. Sodium currents, to somewhat higher concentrations of quinine (IC50 = 6.4 x 10(-5) M), were also reduced in magnitude without noticeable effects on activation or reversal potential but with a shift in inactivation. Calcium currents, visualized with barium as a charge carrier, were enhanced in magnitude by the presence of low concentrations of quinine (10(-5) M) bur were suppressed by higher concentrations (10(-4) M). Quinine broadened the waveform of the gustatory action potential and increased the input resistance. These data serve as genesis to future investigations of the signal transduction mechanism of quinine on voltage-dependent currents.