Maintenance of sodium balance is crucial to mammals and is expressed in the innate salt appetite. With depletion, sodium preference is exaggerated, hypertonic solutions accepted and salt balance restored. This compensatory behaviour is thought to result from a centrally induced change in taste responsiveness. This proposal was tested by recording taste activity from ninety-four single neurones in the nucleus tractus solitarius of sodium-replete (N = 44) and of deprived (N = 50) rats. Twelve Wistar rats were given a nominally sodium-free diet for 10-13 days, and the resulting sodium depletion confirmed by flame photometry of their urine. Nine rats provided control data. Taste stimuli included five concentrations of NaCl (0.003-0.3 M) plus eight other salts, acids, sugars and alkaloids. 2. Taste responsiveness was generally reduced in sodium-depleted rats. Spontaneous activity was 33% lower while responses to sodium salts lagged by a mean of 30%, to acids by 25% and to bitter salts and quinine by 17%. Mean activity to sugars was 60% higher in the deprived group. 3. Activity in sugar- and salt-profile neurones was most affected. In deprived animals responses to sodium salts were lower by 80% among salt-profile cells while among sugar-profile neurones activity to these stimuli was nearly 10 times greater than in controls. These changes in activity resulted in a dramatic shift in the participation of sodium- and sugar-profile cells in the afferent signal for NaCl. In replete animals 60% of sodium-induced activity was transmitted through salt-profile cells while only 1% occurred in sugar-profile neurones. In deprived subjects this situation was nearly reversed as 7% of the total NaCl response was conveyed through salt-profile cells while the contribution of neurones with sugar-profiles rose to 46%. 4. Multidimensional stimulus spaces based on average activity in each of four identifiable neurone subgroups demonstrated a shift in the affiliation of sodium salts away from bitter and acid stimuli and towards sugars. 5. These results confirm earlier findings from the chorda tympani that sodium deprivation suppresses activity evoked by sodium salts. However the application of more recent analytical procedures permits quite a different interpretation of this finding. The overall decrease is merely the net effect of a shift in the major responsibility for encoding sodium from salt-profile neurones to those whose primary sensitivity is to sugars.(ABSTRACT TRUNCATED AT 400 WORDS)
