Appetitive changes during salt deprivation are paralleled by widespread neuronal adaptations in nucleus accumbens, lateral hypothalamus, and central amygdala.

Published

Journal Article

Salt appetite is a goal-directed behavior in which salt-deprived animals ingest high salt concentrations that they otherwise find aversive. Because forebrain areas such as the lateral hypothalamus (LH), central amygdala (CeA), and nucleus accumbens (NAc) are known to play an important role in this behavior, we recorded from these areas while water-deprived (WD) and salt-deprived (SD) rats performed a two-bottle choice test between 0.5 M salt (NaCl) and 0.4 M sucrose. In the SD state, the preference ratio for high molar salt markedly increased. Electrophysiological recordings analyzed with respect to the onset of licking clusters revealed the presence of both excitatory and inhibitory neuronal responses during salt and/or sucrose consumption. In the NAc, putative medium spiny neurons and tonically active neurons exhibited excitatory and inhibitory responses. In all areas, compared with those recorded during the WD state, neurons recorded during the SD state showed an increase in the percentage of salt-evoked excitatory responses and a decrease in the percentage of sucrose-evoked inhibitory responses, suggesting that a subset of the neuronal population in these areas codes for the increased motivational and/or hedonic value of the salt solution. In addition, in the SD state, the firing of excitatory neurons in LH and CeA became more synchronized, indicating a greater functional connectivity between salt-responsive neurons in these areas. We propose that plastic changes in the feeding-related neuronal populations of these forebrain areas arise when changes in metabolic state alter the hedonic and motivational value of a particular taste stimulus.

Full Text

Duke Authors

Cited Authors

  • Tandon, S; Simon, SA; Nicolelis, MAL

Published Date

  • August 2012

Published In

Volume / Issue

  • 108 / 4

Start / End Page

  • 1089 - 1105

PubMed ID

  • 22572944

Pubmed Central ID

  • 22572944

Electronic International Standard Serial Number (EISSN)

  • 1522-1598

Digital Object Identifier (DOI)

  • 10.1152/jn.00236.2012

Language

  • eng

Conference Location

  • United States