Disrupted dentate granule cell chloride regulation enhances synaptic excitability during development of temporal lobe epilepsy. - Wikidata - thesis-toulmin - TriplyDB

Disrupted dentate granule cell chloride regulation enhances synaptic excitability during development of temporal lobe epilepsy.

Disrupted dentate granule cell chloride regulation enhances synaptic excitability during development of temporal lobe epilepsy.

http://www.wikidata.org/entity/Q30481101

about

Role of the neuronal K-Cl co-transporter KCC2 in inhibitory and excitatory neurotransmission GABAergic transmission in temporal lobe epilepsy: the role of neurosteroids.NMDA receptor activity downregulates KCC2 resulting in depolarizing GABAA receptor-mediated currents Depression, stress, epilepsy and adult neurogenesis Neurosteroid replacement therapy for catamenial epilepsy Modulation of neuronal activity by phosphorylation of the K-Cl cotransporter KCC2 Novel determinants of the neuronal Cl(-) concentration A toolbox for spatiotemporal analysis of voltage-sensitive dye imaging data in brain slices Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential Pregabalin attenuates excitotoxicity in diabetes Neurosteroid-sensitive δ-GABAA receptors: A role in epileptogenesis?N-methyl-D-aspartic acid receptor activation downregulates expression of δ subunit-containing GABAA receptors in cultured hippocampal neurons.Surviving hilar somatostatin interneurons enlarge, sprout axons, and form new synapses with granule cells in a mouse model of temporal lobe epilepsy.Excessive activation of mTOR in postnatally generated granule cells is sufficient to cause epilepsy.Decreased CREB levels suppress epilepsy Massively augmented hippocampal dentate granule cell activation accompanies epilepsy development.Small-molecule screen identifies inhibitors of the neuronal K-Cl cotransporter KCC2 Neurogliaform cells in the molecular layer of the dentate gyrus as feed-forward γ-aminobutyric acidergic modulators of entorhinal-hippocampal interplay.KCC2 downregulation facilitates epileptic seizures.Reorganization of inhibitory synaptic circuits in rodent chronically injured epileptogenic neocortex.Impairment of kindling development in phospholipase Cγ1 heterozygous mice.Disruption of TrkB-mediated phospholipase Cgamma signaling inhibits limbic epileptogenesis Neuronal chloride accumulation and excitatory GABA underlie aggravation of neonatal epileptiform activities by phenobarbital.The transcription factor NRSF contributes to epileptogenesis by selective repression of a subset of target genes.GABAA receptor modulation by neurosteroids in models of temporal lobe epilepsies.Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction.Neuroanatomical clues to altered neuronal activity in epilepsy: from ultrastructure to signaling pathways of dentate granule cells.Computational modeling reveals dendritic origins of GABA(A)-mediated excitation in CA1 pyramidal neurons.Prevention or modification of epileptogenesis after brain insults: experimental approaches and translational research.GABAA receptor subtype involvement in addictive behaviour.Genetic controls balancing excitatory and inhibitory synaptogenesis in neurodevelopmental disorder models.Progressive NKCC1-dependent neuronal chloride accumulation during neonatal seizures.Cation-chloride cotransporters in neuronal development, plasticity and disease GABAA receptor trafficking-mediated plasticity of inhibitory synapses.Loss of cation-chloride cotransporter expression in preterm infants with white matter lesions: implications for the pathogenesis of epilepsy Is plasticity of GABAergic mechanisms relevant to epileptogenesis?KCC2 activity is critical in limiting the onset and severity of status epilepticus.Acute and chronic efficacy of bumetanide in an in vitro model of posttraumatic epileptogenesis.Possible alterations in GABAA receptor signaling that underlie benzodiazepine-resistant seizures.Altered inhibition in tuberous sclerosis and type IIb cortical dysplasia.

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P2860

Disrupted dentate granule cell chloride regulation enhances synaptic excitability during development of temporal lobe epilepsy.

http://www.wikidata.org/entity/Q30481101

description

2007 nî lūn-bûn

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2007 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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type

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Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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prefLabel

Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

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JNEUROSCI.4390-07.2007

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Journal of Neuroscience

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Disrupted dentate granule cell ...... ent of temporal lobe epilepsy.

@en

P2093

Douglas A Coulter

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

Florian Weissinger

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Fu-Chun Hsu

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

Gregory C Carlson

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Hemal R Pathak

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Miho Terunuma

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Stephen J Moss

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P2860

KCC2 expression in immature rat cortical neurons is sufficient to switch the polarity of GABA responses

BDNF-induced TrkB activation down-regulates the K+-Cl- cotransporter KCC2 and impairs neuronal Cl- extrusion

Deafness and imbalance associated with inactivation of the secretory Na-K-2Cl co-transporter

Molecular characterization of a putative K-Cl cotransporter in rat brain. A neuronal-specific isoform

The K+/Cl- co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation

Cl- uptake promoting depolarizing GABA actions in immature rat neocortical neurones is mediated by NKCC1

Reduction of KCC2 expression and GABAA receptor-mediated excitation after in vivo axonal injury

The dentate gyrus as a control point for seizures in the hippocampus and beyond.

Massive and specific dysregulation of direct cortical input to the hippocampus in temporal lobe epilepsy.

On the origin of interictal activity in human temporal lobe epilepsy in vitro.

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14012-14022

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10.1523/JNEUROSCI.4390-07.2007

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51

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18094240

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2211568

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