Recent studies have shown that taste cells transducing bitter, sweet, and umami stimuli do not possess high-threshold voltage-gated calcium channels required for synaptic transmission at conventional synapses, suggesting some sort of signal processing inside taste buds prior to the activation of nerve endings. To evaluate whether this is a general paradigm for the physiology of taste reception, we studied the transduction pathway underlying the detection of sodium ions (salty stimulus). In laboratory rodents, Na⁺ is thought to be transduced, at least in part, through amiloride-sensitive sodium channels (ASSCs). Therefore, we used the patch-clamp techniques to analyze the occurrence pattern of amiloride-sensitive sodium currents and voltage-gated calcium currents (both low-voltage-activated T-type current and high-voltage-activated L-type current) among taste cells in rat fungiform papillae. Since taste cells turnover, we focused our attention on cells possessing large voltage-gated sodium currents, a sign of mature cells. We found that cells expressing functional ASSCs either did not possess any calcium currents or exhibited only T-type calcium currents, which is believed to play a role in repetitive firing. On the contrary, cells lacking functional ASSCs were endowed with L-Type calcium currents, which are thought to mediate calcium influx required for neurotransmitter exocytosis. Therefore, our data suggest that sodium-detecting cells are unlikely to use conventional synaptic communication to transfer taste information to nerve endings. Our findings on sodium taste detection support the recent model of taste transduction, involving separate groups of taste cells: chemosensitive cells and cells forming conventional synapses.