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Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice

Smith, Craig M., Walker, Lesley L., Leeboonngam, Tanawan, McKinley, Michael J., Denton, Derek A. and Lawrence, Andrew J. 2016, Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice, Proceedings of the national academy of sciences of the United States of America, vol. 113, no. 48, pp. 13893-13898, doi: 10.1073/pnas.1616664113.

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Title Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice
Author(s) Smith, Craig M.
Walker, Lesley L.
Leeboonngam, Tanawan
McKinley, Michael J.
Denton, Derek A.
Lawrence, Andrew J.
Journal name Proceedings of the national academy of sciences of the United States of America
Volume number 113
Issue number 48
Start page 13893
End page 13898
Total pages 6
Publisher National Academy of Sciences
Place of publication Washington, D.C.
Publication date 2016-11-29
ISSN 0027-8424
1091-6490
Keyword(s) central amygdala
mu-opioid receptor
sodium appetite
Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
SALT APPETITE
CENTRAL NUCLEUS
SOLITARY TRACT
SALINE INTAKE
RATS
ACTIVATION
REWARD
NACL
ALDOSTERONE
PROJECTIONS
Summary Due 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.
Language eng
DOI 10.1073/pnas.1616664113
Field of Research MD Multidisciplinary
Socio Economic Objective 920411 Nutrition
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2016, National Academy of Sciences
Persistent URL http://hdl.handle.net/10536/DRO/DU:30091655

Document type: Journal Article
Collection: School of Social and International Studies
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