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Haloperidol causes cytoskeletal collapse in N1E-115 cells through tau hyperphosphorylation induced by oxidative stress: Implications for neurodevelopment

dc.creatorBenítez-King, Gloria
dc.creatorOrtíz-López, Leonardo
dc.creatorJiménez-Rubio, Graciela
dc.creatorRamírez-Rodríguez, Gerardo
dc.date.accessioned2017-06-30T03:42:32Z
dc.date.available2017-06-30T03:42:32Z
dc.date.issued2010es_ES
dc.identifier2145es_ES
dc.identifier.issn0014-2999es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6800
dc.identifier.urihttps://doi.org/10.1016/j.ejphar.2010.06.057es_ES
dc.language.isoenges_ES
dc.publisherELSEVIER SCIENCE BV, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDSes_ES
dc.relation644 (1) 24-31 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleHaloperidol causes cytoskeletal collapse in N1E-115 cells through tau hyperphosphorylation induced by oxidative stress: Implications for neurodevelopmentes_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartamento de Neurofarmacología, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México, D.F., Méxicoes_ES
dc.contributor.emailbekin@imp.edu.mxes_ES
dc.relation.jnabreviadoEUR J PHARMACOLes_ES
dc.relation.journalEuropean Journal of Pharmacologyes_ES
dc.identifier.placeAmsterdames_ES
dc.date.published2010es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México.es_ES
dc.identifier.eissn1879-0712es_ES
dc.identifier.doi10.1016/j.ejphar.2010.06.057es_ES
dc.description.monthJunes_ES
dc.description.abstractotrodiomaHaloperidol a typical antipsychotic commonly used in the treatment of schizophrenia causes neuronal damage and extrapiramidal symptoms after several years of treatment. These symptoms have been associated with increased levels of oxidative stress. Reactive oxygen species produce cytoskeletal collapse and an excessive phosphorylation of tau, a microtubule-associated protein that plays a key role in microtubule stabilization, and in growth cone and neurite formation, which are cytoskeletal phenotypes that participate in neurodevelopment. Thus, we hypothesized that haloperidol produces neurocytoskeletal disorganization by increasing free radicals and tau hyperphosphorylation, and consequently, the loss of neurodevelopmental cytoskeletal phenotypes, neurites and growth cones. The purpose of this work was the characterization of neuronal cytoskeletal changes caused by haloperidol in neuroblastoma N1E-115 cells. We also studied the mechanisms by which haloperidol causes cytoskeletal changes. The results showed that haloperidol at 100 ?M caused a complete cytoskeleton collapse in the majority of the cells. Melatonin, a free radical scavenger, blocks tau hyperphosphorylation, and microtubule disorganization caused by haloperidol in a dose–response mode. Additionally, the indole blocks lipoperoxide formation in haloperidol treated cells. The results indicate that free radicals and tau hyperphosphorylation produced by haloperidol caused a cytoskeletal collapse and the lost of growth cones and neurites. These effects were blocked by melatonin. Data suggest that extrapiramidal symptoms in schizophrenic patients can be produced by cytoskeletal disorganization during adult brain neurodevelopment after prolonged haloperidol treatment that can be prevented by melatonin.es_ES
dc.subject.kwHaloperidoles_ES
dc.subject.koHaloperidoles_ES
dc.subject.koCytoskeletales_ES
dc.subject.koNeuriteses_ES
dc.subject.koGrowth coneses_ES
dc.subject.koNeurodevelopmentes_ES
dc.subject.koMelatonines_ES


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