Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain. - Wikidata - awgldk - TriplyDB

Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain.

Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain.

http://www.wikidata.org/entity/Q36993407

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A review on alcohol: from the central action mechanism to chemical dependency Lithium-mediated protection against ethanol neurotoxicity JNK pathway activation is controlled by Tao/TAOK3 to modulate ethanol sensitivity Impact of anaesthetics and surgery on neurodevelopment: an update.The neurotrophic and neuroprotective effects of psychotropic agents.Dysregulation of TrkB phosphorylation and proBDNF protein in adenylyl cyclase 1 and 8 knockout mice in a model of fetal alcohol spectrum disorder Focus on apoptosis to decipher how alcohol and many other drugs disrupt brain development.Potential molecular and cellular mechanism of psychotropic drugs Pre-administration of G9a/GLP inhibitor during synaptogenesis prevents postnatal ethanol-induced LTP deficits and neurobehavioral abnormalities in adult mice.Enhanced deficits in long-term potentiation in the adult dentate gyrus with 2nd trimester ethanol consumption.Ethanol exposure induces neonatal neurodegeneration by enhancing CB1R Exon1 histone H4K8 acetylation and up-regulating CB1R function causing neurobehavioral abnormalities in adult mice.Lithium prevents long-term neural and behavioral pathology induced by early alcohol exposure Choline Ameliorates Deficits in Balance Caused by Acute Neonatal Ethanol Exposure.Ketamine-induced neuroapoptosis in the fetal and neonatal rhesus macaque brain.Neuropathological sequelae of developmental exposure to antiepileptic and anesthetic drugs.Lithium Protects Against Anaesthesia Neurotoxicity In The Infant Primate Brain Low-level lead exposure triggers neuronal apoptosis in the developing mouse brain Anandamide-CB1 receptor signaling contributes to postnatal ethanol-induced neonatal neurodegeneration, adult synaptic, and memory deficits Lithium protects against anesthesia-induced developmental neuroapoptosis.Alcohol-induced apoptosis of oligodendrocytes in the fetal macaque brain.Lithium protects against glucocorticoid induced neural progenitor cell apoptosis in the developing cerebellum.Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development.Isoflurane-induced neuroapoptosis in the neonatal rhesus macaque brain.Developmental neurotoxicity of alcohol and anesthetic drugs is augmented by co-exposure to caffeine.The emerging role of dopamine-glutamate interaction and of the postsynaptic density in bipolar disorder pathophysiology: Implications for treatment.Lithium protects against oxidative stress-mediated cell death in α-synuclein-overexpressing in vitro and in vivo models of Parkinson's disease.Ethanol and the Developing Brain: Inhibition of Neuronal Activity and Neuroapoptosis.A single day of 5-azacytidine exposure during development induces neurodegeneration in neonatal mice and neurobehavioral deficits in adult mice.Involvement of sphingolipids in ethanol neurotoxicity in the developing brain Safety first, safety at early age: The quagmire of neurotoxicity in paediatric anaesthesia.CaMKII represses transcriptionally active β-catenin to mediate acute ethanol neurodegeneration and can phosphorylate β-catenin.Clonidine abolishes the adverse effects on apoptosis and behaviour after neonatal ketamine exposure in mice.Minocycline protects developing brain against ethanol-induced damage.Developmental Ethanol-Induced Sleep Fragmentation, Behavioral Hyperactivity, Cognitive Impairment and Parvalbumin Cell Loss are Prevented by Lithium Co-treatment.Inhibition of Cortical Activity and Apoptosis Caused by Ethanol in Neonatal Rats In Vivo.Neuroprotective effects of lithium treatment following hypoxic-ischemic brain injury in neonatal rats.Mechanisms and Consequences of Anesthetic-Induced Neuroapoptosis in the Developing Brain

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P2860

Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain.

http://www.wikidata.org/entity/Q36993407

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2008 nî lūn-bûn

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Ethanol causes and lithium pre ...... ERK in the infant mouse brain.

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Ethanol causes and lithium pre ...... ERK in the infant mouse brain.

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Ethanol causes and lithium pre ...... ERK in the infant mouse brain.

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J.NBD.2008.05.009

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Neurobiology of Disease

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Ethanol causes and lithium pre ...... ERK in the infant mouse brain.

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Catherine Creeley

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Chainllie Young

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John W Olney

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Megan M W Straiko

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Stephen A Johnson

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P2860

Antiepileptic drugs and apoptotic neurodegeneration in the developing brain

Intrinsic and extrinsic pathway signaling during neuronal apoptosis: lessons from the analysis of mutant mice

Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain

Cell death: the significance of apoptosis

Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits.

Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo

Apoptosis in the in vivo mammalian forebrain.

Postinsult treatment with lithium reduces brain damage and facilitates neurological recovery in a rat ischemia/reperfusion model.

Lithium blocks the c-Jun stress response and protects neurons via its action on glycogen synthase kinase 3.

Neuroprotective and neurotrophic actions of the mood stabilizer lithium: can it be used to treat neurodegenerative diseases?

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355-360

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3

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