Kainate seizures cause acute dendritic injury and actin depolymerization in vivo. - Wikidata - wikimedia - TriplyDB

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

http://www.wikidata.org/entity/Q30572720

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Future of seizure prediction and intervention: closing the loop Impact of seizures on developing dendrites: implications for intellectual developmental disabilities Direct Imaging of Hippocampal Epileptiform Calcium Motifs Following Kainic Acid Administration in Freely Behaving Mice The mammalian target of rapamycin signaling pathway mediates epileptogenesis in a model of temporal lobe epilepsy CNF1 Enhances Brain Energy Content and Counteracts Spontaneous Epileptiform Phenomena in Aged DBA/2J Mice.Dendrites have a rapid program of injury-induced degeneration that is molecularly distinct from developmental pruning.Silencing microRNA-134 produces neuroprotective and prolonged seizure-suppressive effects Cognitive dysfunction after experimental febrile seizures.The Impact of Electrographic Seizures on Developing Hippocampal Dendrites Is Calcineurin Dependent.Neurite beading is sufficient to decrease the apparent diffusion coefficient after ischemic stroke.Rapamycin Attenuates Acute Seizure-induced Astrocyte Injury in Mice in Vivo.Wortmannin Attenuates Seizure-Induced Hyperactive PI3K/Akt/mTOR Signaling, Impaired Memory, and Spine Dysmorphology in Rats Moderate traumatic brain injury causes acute dendritic and synaptic degeneration in the hippocampal dentate gyrus.Proteomic profiling of the epileptic dentate gyrus.Synchrony in normal and focal epileptic brain: the seizure onset zone is functionally disconnected Changes in microRNA expression in the whole hippocampus and hippocampal synaptoneurosome fraction following pilocarpine induced status epilepticus.Rapamycin reverses status epilepticus-induced memory deficits and dendritic damage.Synchronization from second order network connectivity statistics Progressive brain damage, synaptic reorganization and NMDA activation in a model of epileptogenic cortical dysplasia.Brief seizures cause dendritic injury Prevalence of non-febrile seizures in children with idiopathic autism spectrum disorder and their unaffected siblings: a retrospective cohort study.In Vivo Two-Photon Imaging of Astrocytes in GFAP-GFP Transgenic Mice.Contrasting features of ERK1/2 activity and synapsin I phosphorylation at the ERK1/2-dependent site in the rat brain in status epilepticus induced by kainic acid in vivo.Rapamycin prevents acute dendritic injury following seizures.The brain, seizures and epilepsy throughout life: understanding a moving target.Pharmacologic suppression of oxidative damage and dendritic degeneration following kainic acid-induced excitotoxicity in mouse cerebrum.SIRT5 Deficiency Enhances Susceptibility to Kainate-Induced Seizures and Exacerbates Hippocampal Neurodegeneration not through Mitochondrial Antioxidant Enzyme SOD2.Computational modeling of epilepsy for an experimental neurologist.Stabilizing dendritic structure as a novel therapeutic approach for epilepsy.Rapid hippocampal network adaptation to recurring synchronous activity--a role for calcineurin.Estradiol facilitates the release of neuropeptide Y to suppress hippocampus-dependent seizures.Disruption of normal cytoskeletal dynamics may play a key role in the pathogenesis of epilepsy.Structural plasticity in the dentate gyrus- revisiting a classic injury model.Roles of matrix metalloproteinases and their targets in epileptogenesis and seizures Dendrite injury triggers DLK-independent regeneration.Seeing the forest and the trees: dendritic injury after status epilepticus.Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential.Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus.Matrix metalloproteinases contribute to neuronal dysfunction in animal models of drug dependence, Alzheimer's disease, and epilepsy.Conditional deletion of the NMDA-NR1 receptor subunit gene in the central nucleus of the amygdala inhibits naloxone-induced conditioned place aversion in morphine-dependent mice.

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P2860

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

http://www.wikidata.org/entity/Q30572720

description

2007 nî lūn-bûn

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2007 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի հոտեմբերին 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

@wuu

name

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

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Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

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type

label

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

@ast

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

@en

prefLabel

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

@ast

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

@en

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JNEUROSCI.0983-07.2007

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Journal of Neuroscience

P1476

Kainate seizures cause acute dendritic injury and actin depolymerization in vivo.

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P2093

Lin Xu

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

Ling-Hui Zeng

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

Michael Wong

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

Nicholas R Rensing

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Philip M Sinatra

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Steven M Rothman

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P2860

A role of actin filament in synaptic transmission and long-term potentiation

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

The hippocampal-dentate complex in temporal lobe epilepsy. A Golgi study

Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation

Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP

Long-term in vivo imaging of experience-dependent synaptic plasticity in adult cortex

Transient and persistent dendritic spines in the neocortex in vivo

Genetic determinants of susceptibility to excitotoxic cell death: implications for gene targeting approaches.

In vivo imaging of dendritic spines during electrographic seizures.

Dynamic actin filaments are required for stable long-term potentiation (LTP) in area CA1 of the hippocampus

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11604-11613

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10.1523/JNEUROSCI.0983-07.2007

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