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Physiol Behav. 2005 Dec 15;86(5):747-61. Epub 2005 Oct 25.

A neural systems analysis of the potentiation of feeding by conditioned stimuli.

Author information

1
Johns Hopkins University, 222 Ames Hall, 3400 North Charles St., Baltimore, MD 21218, USA. pch@jhu.edu

Abstract

Associative learning processes play many important roles in the control of food consumption. Although these processes can complement regulatory mechanisms in the control of eating by providing opportunities for the anticipation of upcoming needs, they may also contribute to inappropriate or pathological consumption patterns by overriding internal regulatory signals. In this article, we first review some of the ways in which associative learning can contribute to the control of feeding, and then describe a neural systems analysis of a simple animal model of the control of feeding by Pavlovian-conditioned stimuli (CSs). Food-sated rats increase their food consumption after presentation of CSs that were previously paired with food while the rats were food-deprived. This cue-potentiated feeding is independent of conditioned approach responses, and is at least somewhat specific to the foods associated with those CSs. A series of studies that used neuroanatomical tract tracing, immediate early gene expression, and neurotoxic disconnection lesion techniques implicated circuitry that includes the basolateral complex of the amygdala, the lateral hypothalamus, and the medial prefrontal cortex, but not the amygdala central nucleus, nucleus accumbens, or lateral orbitofrontal cortex, in cue-potentiated feeding. These studies also showed dissociations between cue-potentiated feeding and other learned motivational phenomena that are known to depend on function of amygdala systems. The data suggest that cue-potentiated feeding is uniquely mediated by cortical and amygdalar neurons that directly target the lateral hypothalamus, and thus gain access to hypothalamic neuropeptide and other systems involved in the promotion and suppression of eating.

PMID:
16256152
PMCID:
PMC1455527
DOI:
10.1016/j.physbeh.2005.08.062
[Indexed for MEDLINE]
Free PMC Article
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