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Activation of paraventricular nucleus of hypothalamus 5-HT1A receptor on sodium intake

dc.contributor.authorVilla, Patricia de Souza
dc.contributor.authorde Arruda Camargo, Gabriela Maria Pavan
dc.contributor.authorde Arruda Camargo, Luiz Antonio
dc.contributor.authorSaad, Wilson Abrao
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de São Carlos (UFSCar)
dc.date.accessioned2014-05-20T13:45:43Z
dc.date.available2014-05-20T13:45:43Z
dc.date.issued2007-05-03
dc.description.abstractHypothalamic paraventricular nucleus (PVN) has an important role in the regulation of water and sodium intake. Several researches described the presence of 5-HT1 receptors in the central nervous system. 5-HTIA was one of the prime receptors identified and it is found in the somatodendritic and post-synaptic forms. Therefore, the aim of this study was to investigate the participation of serotonergic 5-HT1A receptors in the PVN on the sodium intake induced by sodium depletion followed by 24 h of deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Rats (280-320 g) were submitted to the implant of cannulas bilaterally in the PVN. 5-HT injections (10 and 20 mu g/0.2 mu l) in the PVN reduced NaCl 1.8% intake. 8-OH-DPAT injections (2.5 and 5.0 fig/0.2 mu l) in the PVN also reduced NaCl 1.8% intake. pMPPF bilateral injections (5-HT1A antagonist) previously to 8-OH-DPAT injections have completely blocked the inhibitory effect over NaCl 1.8% intake. 5-HT1A antagonists partially reduced the inhibitory effect of 5-HT on NaCl 1.8% intake induced by sodium depletion. In contrast, the intake of palatable solution (2% sucrose) under body fluid-replete conditions was not changed after bilateral PVN 8-OH-DPTA injections. The results show that 5HT(1A) serotonergic mechanisms in the PVN modulate sodium intake induced by sodium loss. The finding that sucrose intake was not affected by PVN 5-HT1A activation suggests that the effects of the 5-HT1A treatments on the intake of NaCl are not due to mechanisms producing a nonspecific decrease of all ingestive behaviors. (c) 2006 Elsevier B.V. All rights reserved.en
dc.description.affiliationUNESP, Sch Dent, Dept Physiol, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUniv Fed Sao Carlos, Dept Physiol, BR-13560 Sao Carlos, Brazil
dc.description.affiliationUnespUNESP, Sch Dent, Dept Physiol, BR-14801903 Araraquara, SP, Brazil
dc.format.extent142-147
dc.identifierhttp://dx.doi.org/10.1016/j.regpep.2006.12.002
dc.identifier.citationRegulatory Peptides. Amsterdam: Elsevier B.V., v. 140, n. 3, p. 142-147, 2007.
dc.identifier.doi10.1016/j.regpep.2006.12.002
dc.identifier.issn0167-0115
dc.identifier.urihttp://hdl.handle.net/11449/16106
dc.identifier.wosWOS:000246086400007
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofRegulatory Peptides
dc.relation.ispartofsjr0,512
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.subjectPVNpt
dc.subjectsodium appetitept
dc.subject5-HTpt
dc.subject5-HT1Apt
dc.subjectpMPPVpt
dc.subjectsucrosept
dc.titleActivation of paraventricular nucleus of hypothalamus 5-HT1A receptor on sodium intakeen
dc.typeArtigopt
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
relation.isDepartmentOfPublicationb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isDepartmentOfPublication.latestForDiscoveryb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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