Role of the central opioid system in the inhibition of water and salt intake induced by central administration of IL-1β in rats

Silva, E. De Castro e; Luz, P. A. C.; Magrani, Janeide; Andrade, Luciana Dantas Farias de; Miranda, N.; Pereira, Vanessa; Fregoneze, J.B.

doi:10.1016/j.pbb.2006.02.009

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…We have demonstrated in previous papers that inhibition of water intake by IL-1b is not due to a non-specific general central nervous system depression or to a decrease in locomotor activity (De Castro e Silva et al, 2006;Luz et al, 2006). However, the potency of the effect of peptides from different batches may vary greatly even when originating from the same supplier, resulting in major differences in the magnitude of a specific effect at a given dose.…”

Section: Discussionmentioning

confidence: 93%

“…These receptors are essential for the induction of water intake promoted by isoproterenol injections (Glass et al, 1994) and deprivation-induced water intake in sham drinking rats is significantly reduced by the blockade of mu-opioid receptors (Leventhal and Bodnar, 1996), a pharmacological condition in which water intake in water-deprived rats is also impaired (Bodnar et al, 1995). In our previous papers (Luz et al, 2006;De Castro e Silva et al, 2006), naloxone, a general opioid antagonist that promotes a significant blockade of mu-opioid receptors, also reduced the antidipsogenic and antinatriorexigenic effects of IL-1b. Hence, it is possible that these effects of IL-1b may be centrally mediated by both kappaand mu-opioid receptors.…”

Section: Discussionmentioning

confidence: 99%

“…doi:10.1016/j.npep.2008.12.006 have also shown that intracerebroventricular administration of IL-1b decreases salt intake in fluid-deprived and sodium depleted rats. Moreover, in this case, the expression of the antidipsogenic and antinatriorexic effect of IL-1b depends on the activity of brain opioid system since these effects are blocked by treatment with non-specific opioid antagonists (De Castro e Silva et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Luz¹,

Saraiva²,

Almeida³

et al. 2009

Neuropeptides

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Luz¹,

Saraiva²,

Almeida³

et al. 2009

Neuropeptides

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“…Opioids have been associated with IL‐1β in the inhibition of sodium appetite (De Castro e Silva et al . ).…”

Section: Introductionmentioning

confidence: 97%

Participation of α₂‐adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide

Luca

Almeida

David

et al. 2015

The Journal of Physiology

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Sickness BehaviourReduced activity and energy shift Abstract Sickness behaviour, a syndrome characterized by a general reduction in animal activity, is part of the active-phase response to fight infection. Lipopolysaccharide (LPS), an effective endotoxin to model sickness behaviour, reduces thirst and sodium excretion, and increases neurohypophysial secretion. Here we review the effects of LPS on thirst and sodium appetite. Altered renal function and hydromineral fluid intake in response to LPS occur in the context of behavioural reorganization, which manifests itself as part of the syndrome. Recent data show that, in addition to its classical effect on thirst, non-septic doses of LPS injected intraperitoneally produce a preferential inhibition of intracellular thirst versus extracellular thirst. Moreover, LPS also reduced hypertonic NaCl intake in sodium-depleted rats that entered a sodium appetite test. Antagonism of α 2 -adrenoceptors abolished the effect of LPS on sodium appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and α 2 -adrenoceptors to control sodium appetite and sickness behaviour. Abstract figure legend Schematic diagram focused on acute-phase responses to LPS, hyperthermia and sickness behaviour. As discussed in the text, reorganization of different behaviours converges to general reduction in activity and energy shift to maintain hyperthermia and fever. Volume conservation mechanisms involving the kidneys and salivary glands may compensate the reduced ingestion of water and sodium. We suggest that reduced sodium appetite belongs to the syndrome as part of sickness behaviour. The diagram also emphasizes brain α2-adrenoceptors and their role to inhibit sodium appetite, or other ingestive behaviours such as sugar intake. LPSAbbreviations CEA, central nucleus of the amygdala; DSAP, saporin toxin conjugated to an antibody against dopamine-β-hydroxylase; DVC, dorsal vagal complex; Furo/Cap, furosemide combined with a low dose of captopril; IL-1β, interleukin-1β; LPBN, lateral parabrachial nucleus; LPS, lipopolysaccharide; MIF, macrophage migration inhibitory factor; NF-κB, nuclear transcription factor kappa B; PVN, hypothalamic paraventricular nucleus; RX821002, methoxy-idazoxan; TLR, Toll-like receptor; TNFα, tumour necrosis factor-α.

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The gut-brain axis and sodium appetite: Can inflammation-related signaling influence the control of sodium intake?

et al. 2022

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Role of the central opioid system in the inhibition of water and salt intake induced by central administration of IL-1β in rats

Cited by 9 publications

References 37 publications

Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Participation of α₂‐adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide

The gut-brain axis and sodium appetite: Can inflammation-related signaling influence the control of sodium intake?

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Role of the central opioid system in the inhibition of water and salt intake induced by central administration of IL-1β in rats

Cited by 9 publications

References 37 publications

Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Blockade of central kappa-opioid receptors inhibits the antidipsogenic effect of interleukin-1β

Participation of α2‐adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide

The gut-brain axis and sodium appetite: Can inflammation-related signaling influence the control of sodium intake?

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Product

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Participation of α₂‐adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide