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Salt Appetite, and the Influence of Opioids

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Abstract

Due to the biological importance of sodium and its relative scarcity within many natural environments, ‘salt appetite’ has evolved whereby dietary salt is highly sought after and palatable when tasted. In addition to peripheral responses, salt depletion is detected within the brain via circumventricular organs and 11β-hydroxysteroid dehydrogenase type 2 (HSD2) neurons to increase salt appetite. Salt appetite is comprised of two main components. One component is the incentive salience or motivation for salt (i.e. how much salt is ‘wanted’). Incentive salience is dynamic and largely depends on internal homeostatic conditions in combination with the detection of relevant cues. It involves the mesolimbic system and structures such as the central amygdala, and opioid signalling within these regions can increase salt intake in rodents. A second key feature is the hedonic palatability of salt (i.e. how much it is ‘liked’) when it is tasted. After detection on the tongue, gustatory information passes through the brainstem nucleus of the solitary tract and thalamus, before being consciously detected within the gustatory cerebral cortex. The positive or negative hedonic value of this stimulus is also dynamic, and is encoded by a network including the nucleus accumbens, ventral pallidum, and lateral parabrachial nucleus. Opioid signalling within these areas can alter salt intake, and ‘liking’. The overconsumption of dietary salt likely contributes to hypertension and associated diseases, and hence further characterising the role played by opioid signalling has important implications for human health.

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Abbreviations

AT1a:

Angiotensin II receptor type 1a

ACE:

Angiotensin-converting enzyme

AgRP:

Agouti-related peptide

CCK:

Cholecystokinin

CeA:

Central amygdala

CGRP:

Calcitonin gene-related peptide

CN:

Cranial nerve

CRF:

Corticotrophin releasing factor

CVO:

Circumventricular organ

DBH:

Dopamine β-hydroxylase

DREADDs:

Designer receptors exclusively activated by designer drugs

HSD2:

11β-Hydroxysteroid dehydrogenase type 2

LPBN:

Lateral parabrachial nucleus

MOR:

Mu-opioid receptor

NAc:

Nucleus accumbens

NTS:

Nucleus of the solitary tract

PBN:

Parabrachial nucleus

VP:

Ventral pallidum

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Acknowledgements

This research was supported by National Health and Medical Research Council of Australia Project Grant APP1079891 (to AJL) and Research Fellowship APP1116930 (to AJL), plus the Victorian Government Operational Infrastructure Support Programme.

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Correspondence to Andrew J. Lawrence.

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Smith, C.M., Lawrence, A.J. Salt Appetite, and the Influence of Opioids. Neurochem Res 43, 12–18 (2018). https://doi.org/10.1007/s11064-017-2336-3

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