dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorDe Luca Junior, Laurival Antonio
dc.creatorAlmeida, Roberto Lopes de
dc.creatorDavid, Richard Boarato
dc.creatorPaula, Patricia Maria de
dc.creatorAndrade, Carina Aparecida Fabrício de
dc.creatorMenani, José Vanderlei
dc.date2015-12-07T15:32:29Z
dc.date2016-10-25T21:22:57Z
dc.date2015-12-07T15:32:29Z
dc.date2016-10-25T21:22:57Z
dc.date2015
dc.date.accessioned2017-04-06T09:28:16Z
dc.date.available2017-04-06T09:28:16Z
dc.identifierThe Journal Of Physiology, 2015.
dc.identifier1469-7793
dc.identifierhttp://hdl.handle.net/11449/131194
dc.identifierhttp://acervodigital.unesp.br/handle/11449/131194
dc.identifier10.1113/JP270377
dc.identifier26036817
dc.identifierhttp://dx.doi.org/10.1113/JP270377
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/941734
dc.descriptionSickness 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.
dc.languageeng
dc.relationThe Journal Of Physiology
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.titleParticipation of α2 -adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide
dc.typeOtro


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