In mammals, transduction of sodium stimuli occurs via amiloride-sensitive sodium channels. In rat, gustatory physiological sensitivity to sodium stimuli develops gradually during the early postnatal period. In addition, if pregnant rats are subjected to dietary sodium restriction during gestation, their offspring fail to develop normal gustatory physiological responses to sodium and sensitivity to amiloride. In the present study, we used polyclonal antibodies raised against amiloride-sensitive sodium channels to ascertain whether gustatory function is correlated with the immunological presence of the transduction apparatus for sodium stimuli in the taste buds of neonatal rats and adult offspring of sodium-restricted dams. The results indicate that antiamiloride-sensitive sodium channel antisera bind cells within taste buds of neonatal and adult rats, regardless of maternal dietary condition. Therefore, despite the functional absence of taste system amiloride-sensitive sodium channels, the antigenic determinants of these channels are expressed. These data suggest that the onset of normal gustatory sodium sensitivity in neonatal normal rats results from the progressive activation of existing, quiescent channels. Furthermore, they rule out the possibility that the failure to synthesize channel protein underlies the lack of gustatory sodium and amiloride sensitivity in the offspring of sodium-restricted rats.