Deficits in NaCl ingestion after damage to the central nucleus of the amygdala in the rat.
These studies examined the NaCl intake behaviors of rats with bilateral electrolytic lesions of the central nucleus of the amygdala (CeAX). Daily need-free intake of 3% NaCl was abolished by CeAX even in rats in which it had been enhanced preoperatively by a history of repeated sodium depletions but was slightly restored by three successive postoperative sodium depletions. CeAX rats drank water but not 3% NaCl to high doses of DOCA and to the activation of cerebral angiotensin II, and expressed small but reliable salt intake (need-induced salt intake or salt appetite) after postoperative sodium depletions. Other ingestive behaviors (water drinking, intake of food and 5% sucrose) were normal. When given decreasing concentrations of NaCl solution the CeAX rats rejected them until the concentration reached 0.2%. These findings suggest that lesions to the central nucleus of the amygdala produce a global impairment in salt intake behaviors that is possibly due to an alteration in the central processing of the salt taste signal.
Galaverna
O
O
University of Pennsylvania, Department of Biology, Philadelphia 19104-6018.
De Luca
L A
LA
Schulkin
J
J
Yao
S Z
SZ
Epstein
A N
AN
D000679:Amygdala / Q000502:physiology*; D000804:Angiotensin II / Q000096:biosynthesis; D000818:Animals; D003900:Desoxycorticosterone / Q000502:physiology; D006400:Hematocrit; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000172:deficiency*; D012982:Sodium, Dietary / Q000008:administration & dosage*; D013395:Sucrose / Q000494:pharmacology; D013649:Taste / Q000187:drug effects
D012982:Sodium, Dietary; D000804:Angiotensin II; D003900:Desoxycorticosterone; D013395:Sucrose; D012964:Sodium