Role of the central nucleus of the amygdala and bed nucleus of the stria terminalis in experimentally-induced salt appetite.

The contributions of the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BST) to salt appetite were evaluated with two treatments which induce sodium chloride (NaCl) ingestion. Cumulative 3 h intakes of 2% NaCl after sodium depletion using furosemide, or subcutaneous (s.c.) injections of yohimbine (YOH), were measured in male, Sprague-Dawley rats both before and after electrolytic lesions of the CeA or the BST. Before surgery, sham-lesion and lesion groups drank equivalent amounts of 2% NaCl in response to furosemide depletion and YOH treatment. After surgery, rats with sham lesions increased their intakes of 2% NaCl following YOH while rats with CeA or BST lesions showed significant decreases. Rats with CeA or BST lesions also showed significant decreases in their intake of 2% NaCl after furosemide depletion, while intakes of the sham lesion groups remained unchanged. Lesions of either nucleus virtually eliminated 24 h need-free salt intake. Before and after surgery, all groups drank equivalent amounts of water in response to s.c. angiotensin II and to s.c. hypertonic saline, indicating the lesions specifically affected salt appetite. The results indicate that the CeA and the BST may be important sites for processing inputs mediating salt appetite.