Lateral parabrachial nucleus and central amygdala in the control of sodium intake

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dc.contributor.authorAndrade-Franze, G. M. F. [UNESP]
dc.contributor.authorAndrade, Carina Aparecida Fabrício de [UNESP]
dc.contributor.authorDe Luca, L. A. [UNESP]
dc.contributor.authorPaula, Patricia Maria de [UNESP]
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:46:04Z
dc.date.available2014-05-20T13:46:04Z
dc.date.issued2010-02-03
dc.description.abstractThe lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important areas for the control of sodium appetite. In the present study we investigated the effects of bilateral lesions of the CeA on the facilitation of water and 0.3 M NaCl intake produced by the blockade of serotonergic mechanisms or activation of alpha(2)-adrenoceptors with bilateral injections of methysergide or moxonidine, respectively, into the LPBN. Male Holtzman rats (n=5-8) with bilateral sham or electrolytic lesions of the CeA (2 mA; 10 s) and stainless steel cannulas implanted bilaterally in the LPBN were used. In sham rats treated with the diuretic furosemide (10 mg/kg b.w.) combined with the angiotensin converting enzyme inhibitor captopril (5 mg/kg b.w) subcutaneously, bilateral injections of moxonidine (0.5 nmol) or methysergide (4 mu g) into the LPBN increased 0.3 M NaCl intake (29.8 +/- 5.1 and 19.5 +/- 3.7 ml/2 h, respectively, versus vehicle: 8.3 +/- 1.4 ml/2 h) and water intake (17.9 +/- 3.7 and 23.3 +/- 2.8 ml/2 h, respectively, versus vehicle: 11.5 +/- 1.6 ml/2 h). Lesions of the CeA (5-18 days) abolished the increase in 0.3 M NaCl and water intake produced by bilateral injections of moxonidine (10.3 +/- 2.8 and 6.8 +/- 2.3 ml/2 h, respectively) and reduced the increase produced by methysergide (13.6 +/- 2.5 and 14.5 +/- 3.2 ml/2 h, respectively) into the LPBN. The present results show that the increase in water and 0.3 M NaCl intake produced by serotonergic blockade and alpha(2)-adrenergic activation in the LPBN depends on the integrity of the CeA, suggesting that facilitatory mechanisms present in the CeA are essential for the increase of water and hypertonic NaCl intake produced by the blockade of the inhibitory mechanisms of the LPBN. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.en
dc.description.affiliationSão Paulo State Univ UNESP, Dept Physiol & Pathol, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Dept Physiol & Pathol, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent633-641
dc.identifierhttp://dx.doi.org/10.1016/j.neuroscience.2009.11.011
dc.identifier.citationNeuroscience. Oxford: Pergamon-Elsevier B.V. Ltd, v. 165, n. 3, p. 633-641, 2010.
dc.identifier.doi10.1016/j.neuroscience.2009.11.011
dc.identifier.issn0306-4522
dc.identifier.lattes0201361251312074
dc.identifier.lattes1023597870118105
dc.identifier.orcid0000-0001-5433-4493
dc.identifier.urihttp://hdl.handle.net/11449/16272
dc.identifier.wosWOS:000274002600001
dc.language.isoeng
dc.publisherPergamon-Elsevier B.V. Ltd
dc.relation.ispartofNeuroscience
dc.relation.ispartofjcr3.382
dc.relation.ispartofsjr1,602
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectsodium appetiteen
dc.subjectparabrachial nucleusen
dc.subjectamygdalaen
dc.subjectthirsten
dc.subjectangiotensin IIen
dc.subjectserotoninen
dc.titleLateral parabrachial nucleus and central amygdala in the control of sodium intakeen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderPergamon-Elsevier B.V. Ltd
unesp.author.lattes0201361251312074[4]
unesp.author.lattes1023597870118105
unesp.author.lattes9055280555067656[2]
unesp.author.orcid0000-0001-5433-4493[4]
unesp.author.orcid0000-0003-1167-4441[5]
unesp.author.orcid0000-0003-3393-2202[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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