Lateral hypothalamus, nucleus accumbens, and ventral pallidum roles in eating and hunger: interactions between homeostatic and reward circuitry
Bilateral lesions of the central nucleus of the amygdala (CeAX) disrupt both need-free and need-induced NaCl intake. Quite surprisingly, in response to sodium depletion, the same rats who fail to augment their NaCl consumption dramatically increase the numbers of oral motor behaviors associated with ingestion that they display when NaCl is presented intraorally. The present study attempts to resolve these apparently contradictory results by measuring the intake of a NaCl solution delivered directly into the mouth. Controls enhanced their intraoral intake of 0.5 M NaCl in response to sodium depletion while CeAX rats did not. CeAX rats, however, showed discriminative intake responses to tastes. Like controls, CeAX rats promptly rejected 0.3 mM quinine infusions and ingested 1.0 M sucrose for prolonged periods. In addition, food deprivation enhanced the intraoral intake of a dilute sucrose solution in both CeAX and control rats. Thus, in the CeAX rat some tastes and some internal states modulate intake as they do in intact rats. These results are consistent with the hypothesis that central nucleus of the amygdala damage interferes with the consummatory phase of NaCl intake behaviors.