Rapid induction of sodium appetite-modifies taste-evoked activity in nucleus tractus solitarius of the rat

When rats are sodium-deprived for a week or more, they develop an enhanced appetite for sodium chloride. This change in behavior is accompanied by modifications in the coding of NaCl by gustatory neurons in the periphery and brainstem. Most commonly, a decreased neural sensitivity to NaCl has been observed, primarily in salt-responsive neurons. A sodium appetite in the absence of need can also be created more rapidly—in less than 15 minutes—by central administration of renin, which replicates the physiological response to sodium deprivation. In the present study, this technique was used in rats to examine how individual neurons in nucleus tractus solitarius (NTS) are affected by the creation of a sodium appetite. Subjects received chronic pretreatment with deoxycorticosterone acetate followed by a pulse infusion of 25 ng of renin into the third ventricle. It was shown in a separate group of rats that this treatment consistently resulted in an elevated preference for NaCl. In rats used for neural recording, infusion of renin was followed by changes in taste-evoked responding to NaCl. Across all neurons, there was a significant decrease in responses to 0.3 and 0.5 M NaCl. Salt-oriented cells also showed this effect, as well as significantly lower responding to 0.1 M NaCl, but only in the 50% of neurons that were most responsive to NaCl prior to infusion. Sugarsensitive neurons, in contrast, showed increased responding during the first second to most NaCl concentrations. These results support earlier studies by confirming that an enhanced salt preference is accompanied by decreased responding to NaCl in salt-sensitive neurons, offset by increased activity in sugar-sensitive cells. Moreover, this effect is shown here to occur in as little as five minutes and to be independent of sodium deficiency.