Amiloride, a blocker of epithelial sodium channels, was found to have significant effects on electrophysiological and behavioral taste responses in the golden hamster (Mesocricetus auratus). Recordings from the whole chorda tympani nerve showed that amiloride rapidly, reversibly, and competitively inhibited responses to NaCl applied to the anterior tongue. The apparent dissociation constant for amiloride binding, extrapolated to zero NaCl concentration, was 10 nM, a value comparable to estimates for various transporting tight epithelia. Recordings from single chorda tympani nerve fibers showed that 10 microM amiloride completely inhibited responses of Na-selective N fibers but had minimal effect on responses of electrolyte-sensitive H fibers, even though both types of fibers responded well to 0.1 M NaCl. Sucrose responses were not affected by amiloride. Addition of 100 microM amiloride to 0.1 M NaCl consistently increased consumption of NaCl in two-bottle drinking tests. These data suggest that one mechanism by which the taste of NaCl is sensed, which does not require adsorption or a second messenger, involves entry of Na+ into taste bud cells through an amiloride-blockable sodium channel. Taste bud cells utilizing this mechanism exclusively activate N fibers, which are involved in the control of NaCl intake. A different mechanism for the detection of NaCl and other electrolytes is utilized by taste bud cells that activate H fibers.