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Author: search.filters.author.Benítez-King, GloriaSubject: search.filters.subject.Melatonin

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    Melatonin: a neurotrophic factor?
    (MDPI, 2022) Miranda-Riestra, Armida; Estrada-Reyes, Rosa; Torres-Sanchez, Erandis D.; Carreño-García, Silvia; Gabriel Ortiz, Genaro; Benítez-King, Gloria; Laboratorio de Neurofarmacología, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calzada México-Xochimilco 101, San Lorenzo Huipulco, Tlalpan 14370, Mexico City, Mexico; genarogabriel@yahoo.com (G.G.O.) ; bekin@imp.edu.mx (G.B.-K.)
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    Further evidence of the melatonin calmodulin interaction: effect on CaMKII activity
    (MDPI, 2022) Argueta, Jesús; Solís-Chagoyán, Héctor; Estrada-Reyes, Rosa; Constantino-Jonapa, Luis A.; Oikawa-Sala, Julián; Velázquez-Moctezuma, Javier; Benítez-King, Gloria; Laboratorio de Neurofarmacología, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calzada México-Xochimilco 101, San Lorenzo Huipulco, Tlalpan, Mexico City 14370, Mexico; bekin@imp.edu.mx, bekin54@hotmail.com ( Gloria Benítez-King)
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    Low doses of ketamine and melatonin in combination produce additive antidepressant-like effects in mice
    (MDPI, 2021) Estrada-Reyes, Rosa; Quero-Chávez, Daniel B.; Trueta, Citlali; Miranda, Armida; Valdés-Tovar, Marcela; Alarcón-Elizalde, Salvador; Oikawa-Sala, Julián; Argueta, Jesús; Constantino-Jonapa, Luis A.; Muñoz-Estrada, Jesús; Dubocovich, Margarita L.; Benítez-King, Gloria; Laboratorio de Fitofarmacología, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calzada México-Xochimilco 101, San Lorenzo Huipulco, Tlalpan, Ciudad de México 14370, Mexico.; bekin@imp.edu.mx; bekin54@hotmail.com (Benítez-King, Gloria)
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    Melatonin rescues the dendrite collapse induced by the pro-oxidant toxin okadaic acid in organotypic cultures of rat hilar hippocampus
    (2020) Solís-Chagoyán, Héctor; Domínguez-Alonso, Aline; Valdés-Tovar, Marcela; Argueta, Jesús; Sánchez-Florentino, Zulay A.; Calixto, Eduardo; Benítez-King, Gloria; Laboratorio de Neurofarmacología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Mexico City 14370, Mexico.; bekin@imp.edu.mx
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    Melatonin supplementation delays the decline of adult hippocampal neurogenesis during normal aging of mice
    (ELSEVIER SCIENCE BV, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS, 2012) Ramírez-Rodríguez, Gerardo; Vega-Rivera, Nelly M.; Benítez-King, Gloria; Castro-García, Mario; Ortíz-López, Leonardo; Laboratory of Neurogenesis, Division of Clinical Research, National Institute of Psychiatry, México, D.F., Mexico; gbernabe@imp.edu.mx
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    ROCK-regulated cytoskeletal dynamics participate in the inhibitory effect of melatonin on cancer cell migration
    (2009) Ortíz-López, Leonardo; Morales-Mulia, Sandra; Ramírez-Rodríguez, Gerardo; Benítez-King, Gloria
    Cell movement is generated by a driving force provided by dynamic cytoskeletal organization. Two main cytoskeletal-dependent features, essential for migration, are the highly cell polarized structure and focal adhesion complexes. Cell migration and substrate anchorage are finely regulated by external signaling exerted by growth factors and hormones. In particular, the serine threonine kinase activated by the small GTPase Rho, the Rho-associated protein kinase (ROCK), participate in both processes through regulation of actin rearrangements in lamellipodia, filopodia, ruffles, and stress fibers. Melatonin, the main product secreted by the pineal gland has oncostatic properties. In MCF-7 cells, 1 nm melatonin reduces migration and invasiveness through increased expression of two cell surface adhesion proteins, E-cadherin and _1-integrin. In this work, we studied the microfilament and microtubule rearrangements elicited by melatonin in migrating leader MCF-7 cells by a wound-healing assay. Additionally, cell anchorage was estimated by quantification of focal adhesions in MCF-7 cells cultured with melatonin. ROCK participation in the indole effects on anchorage and migration was explored by inhibition of the kinase activity with the specific inhibitor of ROCK, the Y-27632 compound. The results indicate that ROCK participates in the melatonin inhibitory effects on cell migration by changing cytoskeletal organization of leader MCF-7 cells. Also, they indicated that indole increased the number of focal contacts through ROCK. These results support the notion that melatonin inhibits cancer cell invasion and metastasis formation via ROCK-regulated microfilament and microtubule organization that converge in a migration/anchorage switch.
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    Haloperidol causes cytoskeletal collapse in N1E-115 cells through tau hyperphosphorylation induced by oxidative stress: Implications for neurodevelopment
    (ELSEVIER SCIENCE BV, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS, 2010) Benítez-King, Gloria; Ortíz-López, Leonardo; Jiménez-Rubio, Graciela; Ramírez-Rodríguez, Gerardo; Departamento de Neurofarmacología, Subdirección de Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México, D.F., México; bekin@imp.edu.mx
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    Melatonin activates PKC-alpha but not PKC-epsilon in N1E-115 cells
    (2001) Benítez-King, Gloria; Hernández, María Eugenia; Tovar, Rosalinda; Ramírez, Gerardo; Departamento de Neurofarmacolog?a, SIC, Instituto Nacional de Psiquiatr?a, Ramon de la Fuente Muñiz, Calz Mexico-Xochimilco No 101, CP 14370, Col. San Lorenzo Huipulco, D.F., Mexico; bekin@imp.edu.mx
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    Neurocytoskeletal Protective Effect of Melatonin: Importance for Morphofunctional Neuronal Polarization
    (2010) Benítez-King, Gloria; Domínguez-Alonso, Aline; Ramírez-Rodríguez, Gerardo; Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calz, México-Xochimilco 101, Col. Sn Lorenzo Huipulco 14370, México, D.F., Mexico; bekin@imp.edu.mx
    Neurons have a highly asymmetric shape and they are constituted by two functional domains: the axonal, and the somatodendritic domains. Axons are cellular processes that make contact with target cells to transmit information, while dendrites located in the somatodendritic domain are specialized in the reception of information. During neurodevelopment, neurons acquire the highly morphofunctional polarization through a dynamic cytoskeletal organization. Melatonin, the main indolamine secreted by the pineal gland has two important properties which play a key role in the maintaining of neuron polarization: it is a potent free radical scavenger, and it is a cytoskeletal modulator. Melatonin stimulates cytoskeletal polarization through PKC and ROCK activation by recruiting cells at early stages of neurodevelopment for later differentiation. At later stages, melatonin induces neurite and microtubule enlargement by a calmodulin antagonism. Moreover, melatonin prevents the asymmetric shape lost induced by oxidative stress, a condition present in neuropsychiatric diseases, and abolishes the cytoskeletal damage caused by prolonged treatment with antipsychotics, restoring the morphofunctional polarization. Moreover, in organotypic cultures, melatonin at nanomolar concentrations enhances the number of dendrites and their complexity in hilar neurons of the hippocampus. In addition, melatonin stimulates the formation of new neurons in vitro and in a rodent model. In this review we will describe current evidences indicative of the melatonin participation in the neuronal morphofunctional differentiation as a cytoskeletal modulator. Also we will discuss the implications of the loss of neuronal polarization in neuropsychiatric diseases and the potential therapeutic utility of melatonin for the treatment of these illnesses.
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    In Vitro Stimulation of Protein Kinase C by Melatonin
    (1998) Antón-Tay, Fernando; Ramírez, Gerardo; Martínez, Isabel; Benítez-King, Gloria; Universidad Autonoma Metropolitana - Iztapalapa, Dpto. de Biología de la Reproducción CBS.; fat@xanum.uam.mx
    It has been shown that melatonin through binding to calmodulin acts both in vitro and in vivo as a potent calmodulin antagonist. It is known that calmodulin antagonists both bind to the hydrophobic domain of Ca2+ activated calmodulin, and inhibit protein kinase C activity. In this work we explored the effects of melatonin on Ca2+ dependent protein kinase C activity in vitro using both a pure commercial rat brain protein kinase C, and a partially purified enzyme from MDCK and N1E-115 cell homogenates. The results showed that melatonin directly activated protein kinase C with a half stimulatory concentration of 1 nM. In addition the hormone augmented by 30% the phorbol ester stimulated protein kinase C activity and increased [3H] PDBu binding to the kinase. In contrast, calmodulin antagonists (500 _M) and protein kinase C inhibitors (100 _M) abolished the enzyme activity. Melatonin analogs tested were ineffective in increasing either protein kinase C activity or [3H] PDBu binding. Moreover, the hormone stimulated protein kinase C autophosphorylation directly and in the presence of phorbol ester and phosphatidylserine. The results show that besides the melatonin binding to calmodulin, the hormone also interacts with protein kinase C only in the presence of Ca2+. They also suggest that the melatonin mechanism of action may involve interactions with other intracellular hydrophobic and Ca2+ dependent proteins.