Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx - Wikidata - awgldk - TriplyDB

Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

http://www.wikidata.org/entity/Q34458296

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Emerging roles of glycogen synthase kinase 3 in the treatment of brain tumors The role of lithium in the treatment of bipolar disorder: convergent evidence for neurotrophic effects as a unifying hypothesis A new look at an old drug: neuroprotective effects and therapeutic potentials of lithium salts Brain oscillations in bipolar disorder and lithium-induced changes Lithium in the treatment of bipolar disorder: pharmacology and pharmacogenetics Mood stabilizers, glycogen synthase kinase-3beta and cell survival Molecular actions and clinical pharmacogenetics of lithium therapy Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition Altered regulation of Akt signaling with murine cerebral malaria, effects on long-term neuro-cognitive function, restoration with lithium treatment FGF-21, a novel metabolic regulator, has a robust neuroprotective role and is markedly elevated in neurons by mood stabilizers Enhanced cell death in MeCP2 null cerebellar granule neurons exposed to excitotoxicity and hypoxia Control of neuronal ion channel function by glycogen synthase kinase-3: new prospective for an old kinase.Mitochondrial dysfunction in bipolar disorder.Neuronal apoptosis induced by pharmacological concentrations of 3-hydroxykynurenine: characterization and protection by dantrolene and Bcl-2 overexpression.Involvment of cytosolic and mitochondrial GSK-3beta in mitochondrial dysfunction and neuronal cell death of MPTP/MPP-treated neurons Beneficial effects of mood stabilizers lithium, valproate and lamotrigine in experimental stroke models.Oxidative stress in early stage Bipolar Disorder and the association with response to lithium A new avenue for lithium: intervention in traumatic brain injury.Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity.Posterior cerebellar vermal deficits in bipolar disorder.Postural control in bipolar disorder: increased sway area and decreased dynamical complexity.Lithium-induced inhibition of Src tyrosine kinase in rat cerebral cortical neurons: a role in neuroprotection against N-methyl-D-aspartate receptor-mediated excitotoxicity.Decreased NR1, NR2A, and SAP102 transcript expression in the hippocampus in bipolar disorder.Neuroplasticity and cellular resilience in mood disorders.Dose-dependent protective effect of lithium chloride on retinal ganglion cells is interrelated with an upregulated intraretinal BDNF after optic nerve transection in adult rats.Emerging trends in the treatment of rapid cycling bipolar disorder: a selected review.Lithium-related genetics of bipolar disorder.Preclinical and clinical investigations of mood stabilizers for Huntington's disease: what have we learned?Potential mechanisms of action of lithium in bipolar disorder. Current understanding.Lithium prevents aberrant NMDA-induced F-actin reorganization in neurons.Neural stem cells and the regulation of neurogenesis in the adult hippocampus Lithium long-term treatment in mood disorders: clinical and genetic predictors.Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments.Neuronal pentraxin 1 induction in hypoxic-ischemic neuronal death is regulated via a glycogen synthase kinase-3α/β dependent mechanism Neuroprotective effects of lithium in cultured cells and animal models of diseases.Glycogen synthase kinase-3beta, mood stabilizers, and neuroprotection.Regulation of ER stress proteins by valproate: therapeutic implications.The neurobiology of treatment response to antidepressants and mood stabilizing medications.Critical role of extracellularly secreted neuronal pentraxin 1 in ischemic neuronal death.The Wnt signaling pathway in bipolar disorder.

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P2860

Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

http://www.wikidata.org/entity/Q34458296

description

1998 nî lūn-bûn

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1998 թուականի Մարտին հրատարակուած գիտական յօդուած

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1998 թվականի մարտին հրատարակված գիտական հոդված

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1998年の論文

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1998年論文

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Chronic lithium treatment robu ...... ceptor-mediated calcium influx

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Chronic lithium treatment robu ...... ceptor-mediated calcium influx

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Chronic lithium treatment robu ...... ceptor-mediated calcium influx

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Proceedings of the National Academy of Sciences of the United States of America

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Chronic lithium treatment robu ...... ceptor-mediated calcium influx

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Chuang DM

http://www.w3.org/2001/XMLSchema#string

Hough CJ

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Nonaka S

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P2860

A molecular mechanism for the effect of lithium on development

Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays

A new generation of Ca2+ indicators with greatly improved fluorescence properties

Glycogen synthase kinase-3: functions in oncogenesis and development

Excitotoxic cell death.

Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function.

In vitro and in vivo inhibition of inositol monophosphatase by the bisphosphonate L-690,330.

Mechanisms of action of anticonvulsants in affective disorders: comparisons with lithium.

Selective release of glutamate from cerebellar granule cells differentiating in culture.

A common denominator linking glycogen metabolism, nuclear oncogenes and development.

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