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Melatonin stimulates dendrite formation and complexity in the hilar zone of the rat hippocampus: participation of the Ca++/Calmodulin complex

dc.creatorDomínguez-Alonso, Aline
dc.creatorValdés-Tovar, Marcela
dc.creatorSolís-Chagoyán, Héctor
dc.creatorBenítez-King, Gloria
dc.date.accessioned2017-06-29T03:58:17Z
dc.date.available2017-06-29T03:58:17Z
dc.date.issued2015es_ES
dc.identifier2817es_ES
dc.identifier.issn1422-0067es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4666
dc.identifier.urihttps://doi.org/10.3390/ijms16011907es_ES
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307341/es_ES
dc.language.isoenges_ES
dc.publisherBasel, Switzerland : MDPIes_ES
dc.relation16 (1) 1907-1927 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleMelatonin stimulates dendrite formation and complexity in the hilar zone of the rat hippocampus: participation of the Ca++/Calmodulin complexes_ES
dc.typeartículoes_ES
dc.contributor.affiliationLaboratorio de Neurofarmacología, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calzada México-Xochimilco No. 101, Col. San Lorenzo-Huipulco, CP 14370 Tlalpan, DF, Mexicoes_ES
dc.contributor.emailaline.dmgzalonso@gmail.comes_ES
dc.relation.jnabreviadoINT J MOL SCIes_ES
dc.relation.journalInternational Journal of Molecular Scienceses_ES
dc.identifier.placeSuizaes_ES
dc.date.published2015es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.doi10.3390/ijms16011907.es_ES
dc.description.monthEnees_ES
dc.description.abstractotrodiomaMelatonin (MEL), the main product synthesized by the pineal gland, stimulates early and late stages of neurodevelopment in the adult brain. MEL increases dendrite length, thickness and complexity in the hilar and mossy neurons of hippocampus. Dendrite formation involves activation of Ca2+/Calmodulin (CaM)-dependent kinase II (CaMKII) by CaM. Previous work showed that MEL increased the synthesis and translocation of CaM, suggesting that MEL activates CaM-dependent enzymes by this pathway. In this work we investigated whether MEL stimulates dendrite formation by CaMKII activation in organotypic cultures from adult rat hippocampus. We found that the CaMKII inhibitor, KN-62, abolished the MEL stimulatory effects on dendritogenesis and that MEL increased the relative amount of CaM in the soluble fraction of hippocampal slices. Also, PKC inhibition abolished dendritogenesis, while luzindole, an antagonist of MEL receptors (MT1/2), partially blocked the effects of MEL. Moreover, autophosphorylation of CaMKII and PKC was increased in presence of MEL, as well as phosphorylation of ERK1/2. Our results indicate that MEL stimulates dendrite formation through CaMKII and the translocation of CaM to the soluble fraction. Dendritogenesis elicited by MEL also required PKC activation, and signaling through MT1/2 receptors was partially involved. Data strongly suggest that MEL could repair the loss of hippocampal dendrites that occur in neuropsychiatric disorders by increasing CaM levels and activation of CaMKII.es_ES
dc.subject.koMelatonines_ES
dc.subject.koDendriteses_ES
dc.subject.koCalmodulin-kinase  IIes_ES
dc.subject.koCalmodulines_ES
dc.subject.koHippocampuses_ES
dc.subject.koNeuropsychiatric  disorderses_ES


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