Navegando por Palavras-chave "Lithium"

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    The contextual fear conditioning deficit presented by spontaneously hypertensive rats (SHR) is not improved by mood stabilizers
    (Elsevier B.V., 2011-08-15) Calzavara, Mariana Bendlin [UNIFESP]; Medrano, Wladimir Agostini [UNIFESP]; Levin, Raquel [UNIFESP]; Libanio, Tania Cristina [UNIFESP]; Ribeiro, Rosana de Alencar [UNIFESP]; Abilio, Vanessa Costhek [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objectives: We have recently reported that spontaneously hypertensive rats (SHR) present a contextual fear conditioning (CFC) deficit. This deficit is improved by antipsychotic drugs, potentiated by proschizophrenia manipulations and not altered by acute administration of carbamazepine, lamotrigine and valproic acid. Nevertheless, the effects of lithium a classical mood stabilizer or repeated treatment with these drugs were not evaluated. the main aim of the present study was to extend our previous work by investigating a possible beneficial effect of acute and/or chronic treatments with lithium or lamotrigine on the acquisition deficit of CFC presented by SHR.Methods: Rats were submitted to CFC task after an acute treatment with lithium and/or a repeated treatment with lithium and lamotrigine.Results: Our data revealed that the CFC deficit presented by SHR is not improved by acute or repeated treatment with lithium. Repeated lamotrigine treatment potentiated the deficit presented by SHR and impaired CFC in control animals (Wistar Rats).Conclusions: These data reinforce the absence of beneficial effects of mood stabilizers on the emotional context processing impairment modeled by SHR. (C) 2011 Elsevier Inc. All rights reserved.
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    Effects of lithium and valproate on oxidative stress and behavioral changes induced by administration of m-AMPH
    (Elsevier B.V., 2012-08-15) da-Rosa, Dayane D.; Valvassori, Samira S.; Steckert, Amanda V.; Ornell, Felipe; Ferreira, Camila L.; Lopes-Borges, Jessica; Varela, Roger B.; Dal-Pizzol, Felipe; Andersen, Monica L. [UNIFESP]; Quevedo, Joao; Univ So Santa Catarina; Universidade Federal de São Paulo (UNIFESP)
    In the last years our research group has studied and validated the animal model of mania induced by dextroamphetamine (D-AMPH). Considering the lack of animal models of mania reported in the literature; this study evaluated the possibilities to validate the animal model induced by methamphetamine (m-AMPH). Then, we evaluated the effects of lithium (Li), valproate (VPA) on the behavior and parameters of oxidative damage in rat brain after administration of m-AMPH. in the prevention treatment, Wistar rats were pretreated with Li. VPA or saline (Sal) for 14 days, and then, between days 8 and 14, rats were treated with m-AMPH (1, 0.5 or 0.25 mg/kg) or Sal. in the reversal treatment, rats were first given m-AMPH (0.25 mg/kg) or Sal. Locomotor behavior was assessed using the open-field task and parameters of oxidative damage were measured in brain structures. Our results show that the hyperactivity was prevented and reverted by Li and VPA only when m-AMPH was administered in the dose of 0.25 mg/kg. in addition, the m-AMPH in all doses administrated induced oxidative damage in both structures tested in two models. Li and VPA reversed and prevented this impairment, however in a way dependent of cerebral area, the dose of m-AMPH and technique. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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    Lithium, a classic drug in psychiatry, improves nilotinib-mediated antileukemic effects
    (Elsevier France-Editions Scientifiques Medicales Elsevier, 2018) Silva, Janaina Peixoto da [UNIFESP]; Calgarotto, Andrana K. [UNIFESP]; Rocha, Katiucha Karolina [UNIFESP]; Santos, Caroline Palmeira dos [UNIFESP]; Smaili, Soraya Soubhi [UNIFESP]; Pereira, Gustavo Jose da Silva [UNIFESP]; Pericole, Fernando Vieira; Duarte, Adriana da Silva Santos; Saad, Sara Teresinha Olalla [UNIFESP]; Bincoletto, Claudia [UNIFESP]
    Although Tyrosine kinase inhibitors (TKIs) that target Bcr-Abl play a key role in Chronic Myeloid Leukemia (CML) therapy, they do not eradicate CML-initiating cells, which lead to the emergence of drug resistance. Here we used the lithium, a GSK-3 inhibitor, to attempt to potentiate the effects of nilotinib against leukemia cells. For this purpose, a K562 leukemia cell line and bone marrow cells from untreated Chronic Myeloid Leukemia (CML) patients, prior to any exposure to TKIs, were used as a model. Our results demonstrated that the combination of lithium + nilotinib (L + N) induced K562-cell death and cleaved caspase-3 when compared to lithium or nilotinib alone, accompanied by GSK-3 beta phosphorylation and Bcr-Abl oncoprotein levels reduction. Interestingly, these events were related to autophagy induction, expressed by increased LC3II protein levels in the group treated with L + N. Furthermore, the clonogenic capacity of progenitor cells from CML patients was drastically reduced by L + N, as well as lithium and nilotinib when used separately. The number of cell aggregates (clusters), were increased by all treatments (L + N, lithium, and nilotinib). This pioneering research has demonstrated that lithium might be of therapeutic value when targeting Bcr-Abl cells with nilotinib because it triggers cell death in addition to exerting classical antiproliferative effects, opening new perspectives for novel target and therapeutic approaches to eradicate CML.
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    Pathophysiology in the comorbidity of Bipolar Disorder and Alzheimer's Disease: pharmacological and stem cell approaches
    (Pergamon-Elsevier Science Ltd, 2018) Correa-Velloso, Juliana C.; Goncalves, Maria C. B. [UNIFESP]; Naaldijk, Yahaira; Oliveira-Giacomelli, Agatha; Pillat, Micheli M.; Ulrich, Henning
    Neuropsychiatric disorders involve various pathological mechanisms, resulting in neurodegeneration and brain atrophy. Neurodevelopmental processes have shown to be critical for the progression of those disorders, which are based on genetic and epigenetic mechanisms as well as on extrinsic factors. We review here common mechanisms underlying the comorbidity of Bipolar Disorders and Alzheimer's Disease, such as aberrant neurogenesis and neurotoxicity, reporting current therapeutic approaches. The understanding of these mechanisms precedes stem cell-based strategies as a new therapeutic possibility for treatment and prevention of Bipolar and Alzheimer's Disease progression. Taking into account the difficulty of studying the molecular basis of disease progression directly in patients, we also discuss the importance of stem cells for effective drug screening, modeling and treating psychiatric diseases, once in vitro differentiation of patient-induced pluripotent stem cells provides relevant information about embryonic origins, intracellular pathways and molecular mechanisms.
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    Successful Combined Therapy with Tamoxifen and Lithium in a Paradoxical Sleep Deprivation-Induced Mania Model
    (Wiley-Blackwell, 2012-01-01) Armani, Fernanda [UNIFESP]; Andersen, Monica L. [UNIFESP]; Andreatini, Roberto; Frussa-Filho, Roberto [UNIFESP]; Tufik, Sergio [UNIFESP]; Fernandes Galduroz, Jose Carlos [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Fed Parana
    Background: Previous studies have suggested that manic states and sleep deprivation could contribute to the pathophysiology of bipolar disorder (BD) through protein kinase C (PKC) signaling abnormalities. Moreover, adjunctive therapy has become a standard strategy in the management of BD patients who respond poorly to current pharmacological treatments. Aim: Thus, the aim of this study was to investigate the possible involvement of PKC inhibition by tamoxifen both separately or in combination with lithium, in paradoxical sleep deprivation (PSD)-induced hyperactivity, one facet of mania-like behavior. Materials & Methods: Adult male C57BL/6J mice were randomly distributed (n = 7/group) in 24-h PSD or control groups and injected intraperitoneally (i.p.) with vehicle, lithium (50, 100, or 150 mg/kg) or tamoxifen (0.5, 1.0, or 2.0 mg/kg experiment 1). in a second experiment, mice were injected i.p. with vehicle or a combination of subeffective doses of lithium and tamoxifen. Animals were subjected to a protocol based on repetitive PSD conditions, followed by assessment of locomotion activity in the open-field task. Results: PSD significantly increased locomotor activity in both experiments. These behavioral changes were prevented by a treatment with lithium or tamoxifen, or a combined treatment with both lithium and tamoxifen. Discussion: Therefore, our findings suggest that lithium and tamoxifen exert reversal effects against PSD-induced hyperactivity in mice. Conclusion: Furthermore, tamoxifen as an adjunct to lithium therapy provides support for an alternative treatment of individuals who either do not respond adequately or cannot tolerate the adverse effects associated with therapeutic doses of lithium.