Na+ appetite induced by depleting extracellular fluid volume activates the enkephalin/mu-opioid receptor system in the rat forebrain

Grondin, M.-E.; Gobeil-Simard, A.; Drolet, Guy; Mouginot, Didier

doi:10.1016/j.neuroscience.2011.06.054

Cited by 13 publications

(8 citation statements)

References 75 publications

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“…However, as the mice used in these Fos studies consumed large volumes of 0.3 M NaCl solution during the 10 min in which access was provided, it is also possible that the observed increase in CeA Fos may be due to indirect stimulation from the mouth and gastrointestinal tract (via the NTS and LPB) to signal the cessation of sodium consumption (30). A similar pattern of Fos immunoreactivity has been reported in rats, where sodium gratification also appeared to approximately double the number of CeA Fos-positive neurons compared with sodium-deficient rats that were killed 24 h after their last furosemide injection (a time point comparable to the present studies in mice) (31). In contrast to the present study, however, sodiumdepleted rats display more Fos immunoreactivity throughout the extended amygdala than sodium-replete controls, including in the central subdivision of the lateral part of the CeA (CeLCn) (19).…”

Section: Discussionsupporting

confidence: 86%

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

Smith

Walker

Leeboonngam

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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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.

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Section: Discussionsupporting

confidence: 86%

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

Smith

Walker

Leeboonngam

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…For example, the accumbens receives multisynaptic input from aldosterone-sensing and sodium-sensing neurons in the hindbrain (Miller and Loewy, 2014; Shekhtman et al, 2007). Sodium depletion alters the level of dopamine transporters and opioid peptides in the accumbens (Grondin et al, 2011; Lucas et al, 2003; Roitman et al, 1999). In addition, sodium depletion modifies the dendritic arbor of ventral striatum neurons (Roitman et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Differential effects of mineralocorticoid and angiotensin II on incentive and mesolimbic activity

Grafe

Flanagan‐Cato

2016

Hormones and Behavior

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The controls of thirst and sodium appetite are mediated in part by the hormones aldosterone and angiotensin II (AngII). The present study examined the behavioral and neural mechanisms of altered effort-value in animals treated with systemic mineralocorticoids, intracerebroventricular AngII, or both. First, rats treated with mineralocorticoid and AngII were tested in the progressive ratio operant task. The willingness to work for sodium versus water depended on hormonal treatment. In particular, rats treated with both mineralocorticoid and AngII preferentially worked for access to sodium versus water compared with rats given only one of these hormones. Second, components of the mesolimbic dopamine pathway were examined for modulation by mineralocorticoids and AngII. Based on cFos immunohistochemistry, AngII treatment activated neurons in the ventral tegmental area and nucleus accumbens, with no enhancement by mineralocorticoid pretreatment. In contrast, western blot analysis revealed that combined hormone treatment increased levels of phospho-tyrosine hydroxylase in the ventral tegmental area. Thus, mineralocorticoid and AngII treatments differentially engaged the mesolimbic pathway based on tyrosine hydroxylase levels versus cFos activation.

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“…The potentiated functional μ‐OR expression in MnPO Na + sensor neurons induced by three repeated Na + depletions might result from either an increased μ‐OR expression or an enhancement in μ‐OR translocation to the membrane. Indeed, a recent study demonstrated that an acute Na + depletion increased the Fos‐immunoreactive and μ‐OR mRNA‐positive neuronal population in the MnPO (Grondin et al ., ). Moreover, it is also possible that the MnPO Na + sensor neurons contain an intracellular pool of μ‐ORs so that repeated Na + depletions might stimulate translocation to the membrane.…”

Section: Discussionmentioning

confidence: 97%

Multiple episodes of sodium depletion in the rat: a remodeling of the electrical properties of median preoptic nucleus neurons

Voisin

Mouginot

Drolet

2013

Eur J of Neuroscience

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In rat brain, the detection and integration of chemosensory and neural signals are achieved, inter alia, by the median preoptic nucleus (MnPO) during a disturbance of the hydromineral balance. This is allowed through the presence of the sodium (Na(+) ) sensor neurons. Interestingly, enkephalins and mu-opioid receptors (μ-ORs) are known for their role in ingestive behaviors and have previously been shown to regulate the excitability of MnPO neurons following a single Na(+) depletion. However, little is known about the role of these μ-ORs in the response enhancement following repeated Na(+) challenge. Therefore, we used whole-cell recordings in acute brain slices to determine neuronal plasticity in the electrical properties of the MnPO Na(+) sensor-specific neuronal population following multiple Na(+) depletions. Our results show that the population of Na(+) sensor neurons was represented by 80% of MnPO neurons after a single Na(+) depletion and was reduced after three Na(+) depletions. Interestingly, the subpopulation of Na(+) sensors responding to D-Ala(2) ,N-MePhe(4) ,Gly-ol-enkephalin (DAMGO), a specific μ-OR agonist, represented 11% of MnPO neurons after a single Na(+) depletion and the population doubled after three Na(+) depletions. Moreover, Na(+) sensor neurons displayed modifications in the discharge pattern distribution and shape of calcium action potentials after three Na(+) depletions but these changes did not occur in Na(+) sensors responding to DAMGO. Thus, the reinforced μ-OR functionality in Na(+) sensors might take place to control the neuronal hyperexcitability and this plasticity in opioid-sensitive and Na(+) detection MnPO networks might sustain the enhanced salt ingestion induced by repeated exposure to Na(+) depletion.

show abstract

Na+ appetite induced by depleting extracellular fluid volume activates the enkephalin/mu-opioid receptor system in the rat forebrain

Cited by 13 publications

References 75 publications

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

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

Differential effects of mineralocorticoid and angiotensin II on incentive and mesolimbic activity

Multiple episodes of sodium depletion in the rat: a remodeling of the electrical properties of median preoptic nucleus neurons

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