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 respond less to hypertonic NaCl than do corresponding cells in replete controls. By administering DOCA and renin, we generated a need-free sodium appetite quickly enough to permit us to monitor the activity of individual neurons in the nucleus of the solitary tract before and after its creation, permitting a more powerful within-subjects design. Subjects received DOCA pretreatment followed by an intracerebroventricular infusion of renin. In animals 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 responsive 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.[1]References
- Rapid induction of sodium appetite modifies taste-evoked activity in the rat nucleus of the solitary tract. McCaughey, S.A., Scott, T.R. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2000) [Pubmed]
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