Artículos de revista

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Author: search.filters.author.Ramírez-Rodríguez, Gerardo

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    Chronic administration of a melatonin membrane receptor antagonist, luzindole, affects hippocampal neurogenesis without changes in hopelessness-like behavior in adult mice
    (Elsevier, 2016) Ortiz-López, Leonardo; Pérez-Beltran, Carlos; Ramírez-Rodríguez, Gerardo; Laboratory of Neurogenesis, Division of Clinical Research, National Institute of Psychiatry "Ramón de la Fuente Muñiz", Calzada México-Xochimilco 101, C.P. 14370, México, D.F., Mexico; gbernabe@imp.edu.mx (G. Ramírez-Rodríguez)
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    Systems genetics analysis of a recombinant inbred mouse cell culture panel reveals Wnt pathway member Lrp6 as a regulator of adult hippocampal precursor cell proliferation
    (Oxford University Press, 2016) Kannan, Suresh; Nicola, Zeina; Overall, Rupert W.; Ichwan, Muhammad; Ramírez-Rodríguez, Gerardo; Grzyb, Anna N.; Patone, Giannino; Saar, Kathrin; Hübner, Norbert; Kempermann, Gerd; CRTD-Center for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden, Germany; gerd.kempermann@dzne.de (Gerd Kempermann)
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    Cannabinoid receptor CB1 mediates baseline and activity-induced survival of new neurons in adult hippocampal neurogenesis
    (2010) Wolf, Susanne A; Bick-Sander, Anika; Fabel, Klaus; Leal-Galicia, Perla; Tauber, Svantje; Ramírez-Rodríguez, Gerardo; Müller, Anke; Melnik, Andre; Waltinger, Tim P; Ullrich, Oliver; Kempermann, Gerd; Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Berlin, Germany; gerd.kempermann@crt-dresden.de
    Background: Adult neurogenesis is a particular example of brain plasticity that is partially modulated by the endocannabinoid system. Whereas the impact of synthetic cannabinoids on the neuronal progenitor cells has been described, there has been lack of information about the action of plant-derived extracts on neurogenesis. Therefore we here focused on the effects of _9-tetrahydrocannabinol (THC) and Cannabidiol (CBD) fed to female C57Bl/6 and Nestin-GFP-reporter mice on proliferation and maturation of neuronal progenitor cells and spatial learning performance. In addition we used cannabinoid receptor 1 (CB1) deficient mice and treatment with CB1 antagonist AM251 in Nestin-GFP-reporter mice to investigate the role of the CB1 receptor in adult neurogenesis in detail. Results: THC and CBD differed in their effects on spatial learning and adult neurogenesis. CBD did not impair learning but increased adult neurogenesis, whereas THC reduced learning without affecting adult neurogenesis. We found the neurogenic effect of CBD to be dependent on the CB1 receptor, which is expressed over the whole dentate gyrus. Similarly, the neurogenic effect of environmental enrichment and voluntary wheel running depends on the presence of the CB1 receptor. We found that in the absence of CB1 receptors, cell proliferation was increased and neuronal differentiation reduced, which could be related to CB1 receptor mediated signaling in Doublecortin (DCX)-expressing intermediate progenitor cells. Conclusion: CB1 affected the stages of adult neurogenesis that involve intermediate highly proliferative progenitor cells and the survival and maturation of new neurons. The pro-neurogenic effects of CBD might explain some of the positive therapeutic features of CBD-based compounds.
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    Acute stress further decreases the effect of ovariectomy on immobility behavior and hippocampal cell survival in rats
    (PERGAMON-ELSEVIER SCIENCE LTD, THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND, 2013) Vega-Rivera, Nelly M.; Fernández-Guasti, Alonso; Ramírez-Rodríguez, Gerardo; Estrada-Camarena, Erika; Laboratory of Neuropsychopharmacology, Division of Neurosciences, National Institute of Psychiatry, Me´xico, D.F., Mexico; estrada@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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    Melatonin Modulates Cell Survival of New Neurons in the Hippocampus of Adult Mice
    (Elsevier Science INC, 360 Park Ave South, New York, NY 10010-1710 USA, 2009) Ramírez-Rodríguez, Gerardo; Klempin, Friederike; Babu, Harish; Benítez-King, Gloria; Kempermann, Gerd; Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Berlin, Germany; gerd.kempermann@crt-dresden.de
    Regulation of adult hippocampal neurogenesis is influenced by circadian rhythm, affected by the manipulation of sleep, and is disturbed in animal models of affective disorders. These observations and the link between dysregulation of the circadian production of melatonin and neuropsychiatric disorders prompted us to investigate the potential role of melatonin in controlling adult hippocampal neurogenesis. In vitro, melatonin increased the number of new neurons derived from adult hippocampal neural precursor cells in vitro by promoting cell survival. This effect was partially dependent on the activation of melatonin receptors as it could be blocked by the application of receptor antagonist luzindole. There was no effect of melatonin on cell proliferation. Similarly, in the dentate gyrus of adult C57BL/6 mice in vivo, exogenous melatonin (8_mg/kg) also increased the survival of neuronal progenitor cells and post-mitotic immature neurons. Melatonin did not affect precursor cell proliferation in vivo and also did not influence neuronal and glial cell maturation. Moreover, melatonin showed antidepressant-like effects in the Porsolt forced swim test. These results indicate that melatonin through its receptor can modulate the survival of newborn neurons in the adult hippocampus, making it the first known exogenously applicable substance with such specificity
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    The α Domain of Small Heat Shock Protein b8 (Hspb8) Acts as Survival and Differentiation Factor in Adult Hippocampal Neurogenesis
    (2013) Ramírez-Rodríguez, Gerardo; Babu, Harish; Klempin, Friederike; Krylyshkina, Olga; Baekelandt, Veerle; Gijsbers, Rik; Debyser, Zeger; Overall, Rupert; Nicola, Zeina; Fabel, Klaus; Kempermann, Gerd; Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calz, México-Xochimilco 101, Col. Sn Lorenzo Huipulco 14370, México, D.F., Mexico; gerd.kempermann@crt-dresden.de
    Adult hippocampal neurogenesis is to a large degree controlled at the level of cell survival, and a number of potential mediators of this effect have been postulated. Here, we investigated the small heat shock protein Hspb8, which, because of its pleiotropic prosurvival effects in other systems, was considered a particularly promising candidate factor. Hspb8 is, for example, found in plaques of Alzheimer disease but exerts neuroprotective effects. We found that expression of Hspb8 increased during differentiation in vitro and was particularly associated with later stages (48–96 h) of differentiation. Gain-of-function and loss-of-function experiments supported the hypothesis that Hspb8 regulates cell survival of new neurons in vitro. In the dentate gyrus of adult mice in vivo, lentiviral overexpression of Hspb8 doubled the surviving cells and concomitantly promoted differentiation and net neurogenesis without affecting precursor cell proliferation. We also discovered that the truncated form of the crystallin domain of Hspb8 was sufficient to affect cell survival and neuronal differentiation in vitro and in vivo. Precursor cell experiments in vitro revealed that Hspb8 increases the phosphorylation of Akt and suggested that the prosurvival effect can be produced by a cell-autonomous mechanism. Analysis of hippocampal Hspb8 expression in mice of 69 strains of the recombinant inbred set BXD revealed that Hspb8 is a cis-acting gene whose expression was associated with clusters of transcript enriched in genes linked to growth factor signaling and apoptosis. Our results strongly suggest that Hspb8 and its _-crystallin domain might act as pleiotropic prosurvival factor in the adult hippocampus.
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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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    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.