Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus - Test2 - elhamkhani - TriplyDB

Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus

Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus

http://www.wikidata.org/entity/Q30498041

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Roles of gap junctions, connexins, and pannexins in epilepsy Role of astrocytes in epilepsy Decreased expression of the glial water channel aquaporin-4 in the intrahippocampal kainic acid model of epileptogenesis.Physiological bases of the K+ and the glutamate/GABA hypotheses of epilepsy.Connexin and pannexin signaling pathways, an architectural blueprint for CNS physiology and pathology?Evidence for aberrant astrocyte hemichannel activity in Juvenile Neuronal Ceroid Lipofuscinosis (JNCL).Laser-scanning astrocyte mapping reveals increased glutamate-responsive domain size and disrupted maturation of glutamate uptake following neonatal cortical freeze-lesion.Sequel of spontaneous seizures after kainic acid-induced status epilepticus and associated neuropathological changes in the subiculum and entorhinal cortex Neuroinflammation alters voltage-dependent conductance in striatal astrocytes.Glutamate biosensor imaging reveals dysregulation of glutamatergic pathways in a model of developmental cortical malformation Astrocyte membrane properties are altered in a rat model of developmental cortical malformation but single-cell astrocytic glutamate uptake is robust.Does brain inflammation mediate pathological outcomes in epilepsy?pH modulation of glial glutamate transporters regulates synaptic transmission in the nucleus of the solitary tract.Gap Junction Blockers: An Overview of their Effects on Induced Seizures in Animal Models.The expression of kainate receptor subunits in hippocampal astrocytes after experimentally induced status epilepticus.Role of gap junctions in epilepsy Understanding the basic mechanisms underlying seizures in mesial temporal lobe epilepsy and possible therapeutic targets: a review.Astrocyte dysfunction in temporal lobe epilepsy: K+ channels and gap junction coupling.Mechanisms underlying blood-brain barrier dysfunction in brain pathology and epileptogenesis: role of astroglia.Contributions of astrocytes to epileptogenesis following status epilepticus: opportunities for preventive therapy?Novel astrocyte targets: new avenues for the therapeutic treatment of epilepsy Glutamatergic Mechanisms Associated with Seizures and Epilepsy.Altered structure and function of astrocytes following status epilepticus."Targeting astrocytes in CNS injury and disease: A translational research approach".Mechanisms of Excessive Extracellular Glutamate Accumulation in Temporal Lobe Epilepsy.Human astrocytes in the diseased brain.Connexins and pannexins: At the junction of neuro-glial homeostasis & disease.Analysis of connexin expression during seizures induced by 4-aminopyridine in the rat hippocampus.Hippocampal Expression of Connexin36 and Connexin43 during Epileptogenesis in Pilocarpine Model of Epilepsy.A cellular network of dye-coupled glia associated with the embryonic central complex in the grasshopper Schistocerca gregaria.Chronic demyelination-induced seizures.Mathematical investigation of IP3-dependent calcium dynamics in astrocytes.N (w) -propyl-L-arginine (L-NPA) reduces status epilepticus and early epileptogenic events in a mouse model of epilepsy: behavioural, EEG and immunohistochemical analyses.Lactation reduces glial activation induced by excitotoxicity in the rat hippocampus.Astrocytic Cx 43 and Cx 40 in the mouse hippocampus during and after pilocarpine-induced status epilepticus.Corneal kindled C57BL/6 mice exhibit saturated dentate gyrus long-term potentiation and associated memory deficits in the absence of overt neuron loss.Astroglial role in the pathophysiology of status epilepticus: an overview.

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Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus

http://www.wikidata.org/entity/Q30498041

description

2010 nî lūn-bûn

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2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年论文

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J.NBD.2010.07.018

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Neurobiology of Disease

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Increased coupling and altered ...... cid-induced status epilepticus

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D K Takahashi

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J R Vargas

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K S Wilcox

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P2860

Cloning and expression of a novel human brain inward rectifier potassium channel

Differential expression of two glial glutamate transporters in the rat brain: quantitative and immunocytochemical observations

Modification of seizure activity by electrical stimulation. II. Motor seizure

Localization of neuronal and glial glutamate transporters

Association between variation in the human KCNJ10 potassium ion channel gene and seizure susceptibility

DL-threo-beta-benzyloxyaspartate, a potent blocker of excitatory amino acid transporters

Conditional knock-out of Kir4.1 leads to glial membrane depolarization, inhibition of potassium and glutamate uptake, and enhanced short-term synaptic potentiation

Kir4.1 expression by astrocytes and oligodendrocytes in CNS white matter: a developmental study in the rat optic nerve

Diverse functions of vertebrate gap junctions

Protoplasmic astrocytes in CA1 stratum radiatum occupy separate anatomical domains

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