Rapid induction of sodium appetite modifies taste-evoked activity in the rat nucleus of the solitary tract

Sodium-deprived rats develop a salt appetite and show changes in gustatory responses to NaCl in the periphery and brain stem; salt-sensitive neurons r espond less to hypertonic NaCl than do corresponding cells in replete contr ols. By administering DOCA and renin, we generated a need-free sodium appet ite quickly enough to permit us to monitor the activity of individual neuro ns in the nucleus of the solitary tract before and after its creation, perm itting a more powerful within-subjects design. Subjects received DOCA pretr eatment followed by an intracerebroventricular infusion of renin. In animal s that were tested behaviorally, this resulted in elevated intake of 0.5 M NaCl. In neural recordings, renin caused decreased responding to hypertonic NaCl across all neurons and in the salt-sensitive neurons that were most r esponsive to NaCl before infusion. Most sugar-sensitive cells, in contrast, gave increased phasic responses to NaCl. These results confirm that sodium appetite is accompanied by decreased responding to NaCl in salt-sensitive neurons, complemented by increased activity in sugar-sensitive cells, even when created rapidly and independently of need.