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Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice
journal contribution
posted on 2016-11-29, 00:00 authored by Craig SmithCraig Smith, L L Walker, T Leeboonngam, M J McKinley, D A Denton, A J LawrenceDue to the importance of dietary sodium and its paucity within many inland environments, terrestrial animals have evolved an instinctive sodium appetite that is commensurate with sodium deficiency. Despite a well-established role for central opioid signaling in sodium appetite, the endogenous influence of specific opioid receptor subtypes within distinct brain regions remains to be elucidated. Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Fos immunohistochemistry revealed discrete regions of the mouse brain displaying an increased number of activated neurons during sodium gratification: the rostral portion of the nucleus of the solitary tract (rNTS), the lateral parabrachial nucleus (LPB), and the central amygdala (CeA). The CeA was subsequently targeted with bilateral infusions of the MOR antagonist naloxonazine, which significantly reduced sodium appetite in mice. The CeA is therefore identified as a key node in the circuit that contributes to sodium appetite. Moreover, endogenous opioids, acting via MOR, within the CeA promote this form of appetitive behavior.
History
Journal
Proceedings of the national academy of sciences of the United States of AmericaVolume
113Issue
48Pagination
13893 - 13898Publisher
National Academy of SciencesLocation
Washington, D.C.Publisher DOI
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ISSN
0027-8424eISSN
1091-6490Language
engPublication classification
C Journal article; C1 Refereed article in a scholarly journalCopyright notice
2016, National Academy of SciencesUsage metrics
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