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

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 α2‐adrenoceptors abolished the effect of LPS on sodium appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and α2‐adrenoceptors to control sodium appetite and sickness behaviour. 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.