Endogenous polyamines regulate cortical neuronal excitability by blocking voltage-gated Na+ channels
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Structural Insight into DFMO Resistant Ornithine Decarboxylase from Entamoeba histolytica: An Inkling to Adaptive EvolutionPhenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation propertiesSpermine synthase.A New Transgenic Mouse Model for Studying the Neurotoxicity of Spermine Oxidase Dosage in the Response to Excitotoxic Injury.Sensitivity of cloned muscle, heart and neuronal voltage-gated sodium channels to block by polyamines: a possible basis for modulation of excitability in vivo.Spatial mismatch between the Na+ flux and spike initiation in axon initial segment.Kainate receptor pore-forming and auxiliary subunits regulate channel block by a novel mechanismMutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitabilityInward-rectifying potassium (Kir) channels regulate pacemaker activity in spinal nociceptive circuits during early life.Polyamines and their metabolites as diagnostic markers of human diseases.Mouse models to investigate the function of spermineMammalian polyamine metabolism and functionNa+ channelopathies and epilepsy: recent advances and new perspectives.Inflammation, carcinogenesis and neurodegeneration studies in transgenic animal models for polyamine research.Targets of polyamine dysregulation in major depression and suicide: Activity-dependent feedback, excitability, and neurotransmission.N(8)-acetylspermidine as a potential plasma biomarker for Snyder-Robinson syndrome identified by clinical metabolomics.Regulation of neuronal excitability by release of proteins from glial cells.Cell-attached single-channel recordings in intact prefrontal cortex pyramidal neurons reveal compartmentalized D1/D5 receptor modulation of the persistent sodium current.Natural product polyamines that inhibit human carbonic anhydrases.Identification of a mammalian vesicular polyamine transporter.Astrocyte-Dependent Vulnerability to Excitotoxicity in Spermine Oxidase-Overexpressing Mouse.Rhythmic intrinsic bursting neurons in human neocortex obtained from pediatric patients with epilepsy.An increase in persistent sodium current contributes to intrinsic neuronal bursting after status epilepticus.A neuroprotective role for polyamines in a Xenopus tadpole model of epilepsy.A new transgenic mouse model for studying the neurotoxicity of spermine oxidase dosage in the response to excitotoxic injury
P2860
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P2860
Endogenous polyamines regulate cortical neuronal excitability by blocking voltage-gated Na+ channels
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Endogenous polyamines regulate ...... ing voltage-gated Na+ channels
@en
type
label
Endogenous polyamines regulate ...... ing voltage-gated Na+ channels
@en
prefLabel
Endogenous polyamines regulate ...... ing voltage-gated Na+ channels
@en
P2093
P2860
P356
P1476
Endogenous polyamines regulate ...... ing voltage-gated Na+ channels
@en
P2093
Efrat Katz
Ilya A Fleidervish
Lior Libman
Michael J Gutnick
P2860
P304
18994-18999
P356
10.1073/PNAS.0803464105
P407
P577
2008-11-19T00:00:00Z