Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
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The pathophysiology of multiple sclerosis: the mechanisms underlying the production of symptoms and the natural history of the diseaseProtective effects of antiarrhythmic agents against anoxic injury in CNS white matterPersistent Sodium Current and Its Role in EpilepsyA prospective, multicenter, phase I matched-comparison group trial of safety, pharmacokinetics, and preliminary efficacy of riluzole in patients with traumatic spinal cord injury.Functional specializations of primary auditory afferents on the Mauthner cells: interactions between membrane and synaptic properties.Axonal L-type Ca2+ channels and anoxic injury in rat CNS white matter.Evoked membrane potential change in rat optic nerve fiber: computer simulation.Sodium channels and pain.Mechanisms of paresthesias arising from healthy axons.The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons.Mechanisms of axonal injury: internodal nanocomplexes and calcium deregulation.Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchangerAnoxic and ischemic injury of myelinated axons in CNS white matter: from mechanistic concepts to therapeutics.Beyond faithful conduction: short-term dynamics, neuromodulation, and long-term regulation of spike propagation in the axon.Quantitative ultrastructural analysis of a single spinal cord demyelinated lesion predicts total lesion load, axonal loss, and neurological dysfunction in a murine model of multiple sclerosisDopamine modulation of Ih improves temporal fidelity of spike propagation in an unmyelinated axonInflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.Sodium channels and multiple sclerosis: roles in symptom production, damage and therapy.Type III sodium channel mRNA is expressed in embryonic but not adult spinal sensory neurons, and is reexpressed following axotomyCa(2+) signaling evoked by activation of Na(+) channels and Na(+)/Ca(2+) exchangers is required for GABA-induced NG2 cell migration.Heteromeric Kv7.2/7.3 channels differentially regulate action potential initiation and conduction in neocortical myelinated axons.White matter injury: Ischemic and nonischemic.Examining protection from anoxic depolarization by the drugs dibucaine and carbetapentane using whole cell recording from CA1 neurons.Membrane trauma and Na+ leak from Nav1.6 channels.Axonal protection achieved by blockade of sodium/calcium exchange in a new model of ischemia in vivoNa(+)-Ca2+ exchange in anoxic/ischemic injury of CNS myelinated axons.Left-shifted nav channels in injured bilayer: primary targets for neuroprotective nav antagonists?Ionic mechanisms maintaining action potential conduction velocity at high firing frequencies in an unmyelinated axon.Characterization of acid-sensing ion channel expression in oligodendrocyte-lineage cells.Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons.Ionic mechanisms of aglycemic axon injury in mammalian central white matter.Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivo.Effects of in situ administration of excitatory amino acid antagonists on rapid microglial and astroglial reactions in rat hippocampus following traumatic brain injury.Subthreshold sodium current underlies essential functional specializations at primary auditory afferents.Breakdown of calcium homeostasis in relation to tissue depolarization: comparison between gray and white matter ischemia.Coupled left-shift of Nav channels: modeling the Na⁺-loading and dysfunctional excitability of damaged axons.Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation.Brain intra- and extracellular sodium concentration in multiple sclerosis: a 7 T MRI study.Temperature dependence of excitability indices of human cutaneous afferents.
P2860
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P2860
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年学术文章
@wuu
1993年学术文章
@zh-cn
1993年学术文章
@zh-hans
1993年学术文章
@zh-my
1993年学术文章
@zh-sg
1993年學術文章
@yue
1993年學術文章
@zh
1993年學術文章
@zh-hant
name
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@ast
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@en
type
label
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@ast
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@en
prefLabel
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@ast
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons.
@en
P2093
P2860
P356
P1476
Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons
@en
P2093
H Sontheimer
S G Waxman
P2860
P304
P356
10.1073/PNAS.90.15.6976
P407
P577
1993-08-01T00:00:00Z