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dc.creatorGalván-Arrieta, Taniaes_ES
dc.creatorTrueta, Citlalies_ES
dc.creatorCercós, Montserrat G.es_ES
dc.creatorValdés-Tovar, Marcelaes_ES
dc.creatorAlarcón, Salvadores_ES
dc.creatorOikawa, Julianes_ES
dc.creatorZamudio-Meza, Horacioes_ES
dc.creatorBenítez-King, Gloriaes_ES
dc.date2017
dc.date.accessioned2021-06-16T15:10:08Z
dc.date.available2021-06-16T15:10:08Z
dc.date.issued2017es_ES
dc.identifierhttps://doi.org/10.1111/jpi.12421es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7462
dc.descriptionDim light exposure of the mother during pregnancy has been proposed as one of the environmental factors that affect the fetal brain development in schizophrenia. Melatonin circulating levels are regulated by the environmental light/dark cycle. This hormone stimulates neuronal differentiation in the adult brain. However, little is known about its role in the fetal human brain development. Olfactory neuronal precur sors (ONPs) are useful for studying the physiopathology of neuropsychiatric diseases because they mimic all the stages of neurodevelopment in culture. Here, we first char acterized whether melatonin stimulates neuronal differentiation in cloned ONPs ob tained from a healthy control subject (HCS). Then, melatonin effects were evaluated in primary cultures of ONPs derived from a patient diagnosed with schizophrenia (SZ) and an age- and gender-matched HCS. Axonal formation was evidenced morphologi cally by tau immunostaining and by GSK3β phosphorylated state. Potassium-evoked secretion was assessed as a functional feature of differentiated neurons. As well, we report the expression of MT1/2 receptors in human ONPs for the first time. Melatonin stimulated axonal formation and ramification in cloned ONPs through a receptor mediated mechanism and enhanced the amount and velocity of axonal and somatic secretion. SZ ONPs displayed reduced axogenesis associated with lower levels of pGSK3β and less expression of melatonergic receptors regarding the HCS ONPs. Melatonin counteracted this reduction in SZ cells. Altogether, our results show that melatonin signaling is crucial for functional differentiation of human ONPs, strongly suggesting that a deficit of this indoleamine may lead to an impaired neurodevelop ment which has been associated with the etiology of schizophrenia.es_ES
dc.formatPDFes_ES
dc.language.isoIngléses_ES
dc.publisherWILEYes_ES
dc.rightsacceso cerradoes_ES
dc.sourceJournal of Pineal Research (1600079X) Vol. 63 no.3 e12421 p.1-16 (2017)es_ES
dc.subjectAxoneses_ES
dc.titleThe role of melatonin in the neurodevelopmental etiology of schizophrenia: A study in human olfactory neuronal precursorses_ES
dc.typeArtículoes_ES
dc.subject.kwMelatoninaes_ES
dc.subject.kwNeurodesarrolloes_ES
dc.subject.kwPrecursores neuronaleses_ES
dc.subject.kwSecreciónes_ES


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