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dc.contributor.authorColombari, Debora S. A.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorFreiria-Oliveira, Andre H. [UNESP]
dc.contributor.authorAntunes, Vagner R.
dc.contributor.authorYao, Song T.
dc.contributor.authorHindmarch, Charles
dc.contributor.authorFerguson, Alastair V.
dc.contributor.authorFry, Mark
dc.contributor.authorMurphy, David
dc.contributor.authorPaton, Julian F. R.
dc.identifier.citationJournal of Physiology-london. Hoboken: Wiley-blackwell, v. 589, n. 18, p. 4457-4471, 2011.
dc.description.abstractWe investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t) SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e. g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed up-regulation of AP1 transcription factor JunD in the dehydrated cNTS, we tested the hypothesis that AP1 transcription factor activity is responsible for dehydration-induced functional plasticity. When AP1 activity was blocked in the cNTS using a viral vector expressing a dominant negative FosB, cNTS inactivation was ineffective. However, tSNA was decreased after pre-collicular transection, a response similar to that seen in EHrats. Thus, the dehydration-induced switch in control of tSNA from hypothalamus to cNTS seems to be mediated via activation of AP1 transcription factors in the cNTS. If AP1 activity is blocked in the cNTS during dehydration, sympathetic activity control reverts back to forebrain regions. This unique reciprocating neural structure-switching plasticity between brain centres emphasizes the multiple mechanisms available for the adaptive response to dehydration.en
dc.relation.ispartofJournal of Physiology-london
dc.sourceWeb of Science
dc.titleSwitching control of sympathetic activity from forebrain to hindbrain in chronic dehydrationen
dc.contributor.institutionUniv Bristol
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionQueens Univ
dc.contributor.institutionUniv Manitoba
dc.description.affiliationUniv Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol BS1 3NY, Avon, England
dc.description.affiliationUniv Bristol, Sch Physiol & Pharmacol, Bristol Heart Inst, Bristol BS9 1TD, Avon, England
dc.description.affiliationSão Paulo State Univ UNESP, Dept Physiol & Pathol, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUniv São Paulo, Dept Physiol & Biophys, Inst Biomed Sci, São Paulo, Brazil
dc.description.affiliationQueens Univ, Dept Physiol, Kingston, on K7L 3N6, Canada
dc.description.affiliationUniv Manitoba, Dept Biol Sci, Winnipeg, MB R3T 2N2, Canada
dc.description.affiliationUnespSão Paulo State Univ UNESP, Dept Physiol & Pathol, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
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