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

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Issued Date

2016

Resource Type

Article

File Type

application/pdf

ISSN

278424

DOI

10.1073/pnas.1616664113

Other identifier(s)

2-s2.0-84999115076

Rights Holder(s)

Scopus

Bibliographic Citation

Proceedings of the National Academy of Sciences of the United States of America. Vol 113, No.48 (2016), p.13893-13898

Suggested Citation

Smith C.M., Walker L.L., Leeboonngam T., Mckinley M.J., Denton D.A., Lawrence A.J. 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 (2016), p.13893-13898. doi:10.1073/pnas.1616664113 Retrieved from: https://hdl.handle.net/20.500.14740/4938

Title

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

Author(s)

Smith C.M.
 Walker L.L.
 Leeboonngam T.
 Mckinley M.J.
 Denton D.A.
 Lawrence A.J.

Abstract

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. © 2016, National Academy of Sciences. All rights reserved.

Subject(s)

Delta opiate receptor
 Morphine
 Mu opiate receptor
 Naloxonazine
 Naltrexone
 Naltrindole
 Protein fos
 Sodium
 Mu opiate receptor
 Naloxone
 Narcotic analgesic agent
 Animal experiment
 Animal tissue
 Article
 Brain region
 Central nucleus (amygdala)
 Controlled study
 Immunohistochemistry
 Immunoreactivity
 Mouse
 Nonhuman
 Parabrachial nucleus
 Priority journal
 Signal transduction
 Sodium appetite
 Sodium intake
 Solitary tract nucleus
 Analogs and derivatives
 Animal
 Antagonists and inhibitors
 Appetite
 Brain mapping
 Central nucleus (amygdala)
 Drug effects
 Genetics
 Metabolism
 Nerve cell
 Physiology
 Signal transduction
 Analgesics, Opioid
 Animals
 Appetite
 Brain Mapping
 Central Amygdaloid Nucleus
 Mice
 Naloxone
 Neurons
 Receptors, Opioid, mu
 Signal Transduction
 Sodium, Dietary

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URI

https://hdl.handle.net/20.500.14740/4938

Collections

Scopus: Year 1983-2021

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