An appetite for CaCl2 and NaCl occurs in young rats after they are fed a diet lacking Ca or Na, respectively. Bilateral lesions of the parabrachial nuclei (PBN) disrupt normal taste aversion learning and essentially eliminate the expression of sodium appetite. Here we tested whether similar lesions of the PBN would disrupt the calcium-deprivation-induced appetite for CaCl2 or NaCl. Controls and rats with PBN lesions failed to exhibit a calcium-deprivation-induced appetite for CaCl2. Nevertheless, both groups did exhibit a significant calcium-deprivation-induced appetite for 0.5M NaCl. Thus, while damage to the second central gustatory relay in the PBN disrupts the appetite for 0.5M NaCl induced by furosemide, deoxycorticosterone acetate, and polyethylene glycol, the sodium appetite induced by dietary CaCl2 depletion remains intact. •Controls and rats with parabrachial lesions (PBNx) failed to ingest 0.5M CaCl2 after extended dietary calcium depletion.•Both groups did ingest significantly more 0.5M NaCl after the same calcium depletion.•Following sodium depletion with a diuretic, the PBNx rats ingested only one-third as much 0.5M NaCl as the Controls.•Damage to the second central gustatory relay in the parabrachial nuclei disrupts an appetite for 0.5 M NaCl in sodium but not calcium depleted rats.
All Science Journal Classification (ASJC) codes
- Experimental and Cognitive Psychology
- Behavioral Neuroscience