Melatonin attenuates tyrosine hydroxylase loss and hypolocomotion in MPTP-lesioned rats

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dc.contributor.authorCapitelli, Caroline
dc.contributor.authorSereniki, Adriana
dc.contributor.authorSantos Lima, Marcelo Meira [UNIFESP]
dc.contributor.authorReksidler, Angela Braga
dc.contributor.authorTufik, Sergio [UNIFESP]
dc.contributor.authorBarbato Frazao Vital, Maria Aparecida
dc.contributor.institutionUniv Fed Parana
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:51:46Z
dc.date.available2016-01-24T13:51:46Z
dc.date.issued2008-10-10
dc.description.abstractParkinson's disease is a chronic neurological disease characterized by dopaminergic neuron degeneration in the substantia nigra pars compacta. Melatonin is a powerful antioxidant agent secreted by the pineal gland which has numerous physiological functions and seems to exert an important neuroprotective effect. the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model has been used to understand the pathophysiology of the disease because of its capacity to mimic biochemical and histological features observed in Parkinson's disease. This study investigated the effect of pretreatment with melatonin (50 mg/kg) on MPTP-lesioned animals 24 h and 7 days after neurotoxin infusion using the open-field test, two-way avoidance task and immunohistochemistry. Twenty-four hours after lesioning, the MPTP+vehicle group exhibited hypolocomotion and significant loss of tyrosine hydroxylase-immunoreactive cells, whereas no differences in these parameters were observed in lesioned animals receiving melatonin. Seven days after surgery, the MPTP-lesioned rats did not show hypolocomotion compared to control animals, while there was a significant dopaminergic neuronal loss. in the two-way avoidance task, MPTP-treated animals presented a cognitive deficit compared to the control groups and melatonin administration did not repair this defect. the present results suggest that melatonin reduces neuronal loss in the MPTP animal model of Parkinson's disease. (C) 2008 Published by Elsevier B.V.en
dc.description.affiliationUniv Fed Parana, Dept Farmacol, Setor Ciencias Biol, BR-81531990 Curitiba, Parana, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Psicobiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Psicobiol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipAFIP
dc.description.sponsorshipIDFAPESP: 06/55968-6
dc.format.extent101-108
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2008.07.022
dc.identifier.citationEuropean Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 594, n. 1-3, p. 101-108, 2008.
dc.identifier.doi10.1016/j.ejphar.2008.07.022
dc.identifier.issn0014-2999
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30965
dc.identifier.wosWOS:000259658300015
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Pharmacology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectactive avoidanceen
dc.subjectcognitive impairmenten
dc.subjectmelatoninen
dc.subjectMPTPen
dc.subjectParkinson's diseaseen
dc.subjecttyrosine hydroxylaseen
dc.titleMelatonin attenuates tyrosine hydroxylase loss and hypolocomotion in MPTP-lesioned ratsen
dc.typeinfo:eu-repo/semantics/article
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