Spontaneously Hypertensive Rats (SHR) present deficits in prepulse inhibition of startle specifically reverted by clozapine

dc.contributor.authorLevin, Raquel [UNIFESP]
dc.contributor.authorCalzavara, Mariana Bendlin [UNIFESP]
dc.contributor.authorSantos, Camila Mauricio [UNIFESP]
dc.contributor.authorMedrano, Wladimir Agostini [UNIFESP]
dc.contributor.authorNiigaki, Suzy Tamie [UNIFESP]
dc.contributor.authorAbilio, Vanessa Costhek [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:17:05Z
dc.date.available2016-01-24T14:17:05Z
dc.date.issued2011-08-15
dc.description.abstractDeficits in an operational measure of sensorimotor gating - the prepulse inhibition of startle (PPI) - are presented in psychiatric disorders such as schizophrenia, bipolar disorder, and attention deficit/hyperactivity disorder (ADHD). Some previous studies showed that the spontaneously hypertensive rats (SHR) present PPI deficit. Although SHR is suggested as an animal model to study ADHD, we have suggested that the behavioral phenotype of this strain mimics some aspects of schizophrenia. the aim of this study was to characterize the PPI response in SHR. Pharmacological characterization consisted in the evaluation of the effects of the following drugs administered to adult Wistar rats (WR) and SHR previously to the PPI test: amphetamine (used for ADHD and also a psychotomimetic drug), haloperidol and clozapine (antipsychotic drugs), metoclopramide (dopamine antagonist without antipsychotic properties) and carbamazepine (mood stabilizer). Our results showed that SHR presented reduced PPI. This deficit was similar to that induced by amphetamine in WR. Only the atypical antipsychotic clozapine improved the PPI deficit observed in SHR. These findings reinforce the SHR strain as an animal model to study several aspects of schizophrenia, including the abnormalities in sensorimotor gating associated with this disease. (C) 2011 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Pharmacol, BR-04039032 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Psychiat, LINC, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Pharmacol, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Psychiat, LINC, BR-04039032 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1748-1752
dc.identifierhttp://dx.doi.org/10.1016/j.pnpbp.2011.06.003
dc.identifier.citationProgress in Neuro-psychopharmacology & Biological Psychiatry. Oxford: Pergamon-Elsevier B.V., v. 35, n. 7, p. 1748-1752, 2011.
dc.identifier.doi10.1016/j.pnpbp.2011.06.003
dc.identifier.fileWOS000294941800033.pdf
dc.identifier.issn0278-5846
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/33956
dc.identifier.wosWOS:000294941800033
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofProgress in Neuro-psychopharmacology & Biological Psychiatry
dc.rightsAcesso aberto
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectSHRen
dc.subjectSchizophreniaen
dc.subjectPrepulse inhibition of startleen
dc.subjectAntipsychoticsen
dc.subjectAmphetamineen
dc.titleSpontaneously Hypertensive Rats (SHR) present deficits in prepulse inhibition of startle specifically reverted by clozapineen
dc.typeResenha
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