Deficits in NaCl ingestion after damage to the central nucleus of the amygdala in the rat

Brain Res Bull. 1992 Jan;28(1):89-98. doi: 10.1016/0361-9230(92)90234-o.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amygdala / physiology*
  • Angiotensin II / biosynthesis
  • Animals
  • Desoxycorticosterone / physiology
  • Hematocrit
  • Male
  • Rats
  • Rats, Inbred Strains
  • Sodium / deficiency*
  • Sodium, Dietary / administration & dosage*
  • Sucrose / pharmacology
  • Taste / drug effects

Substances

  • Sodium, Dietary
  • Angiotensin II
  • Desoxycorticosterone
  • Sucrose
  • Sodium