Published in Lancet Neurol on September 01, 2003
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De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP. Am J Hum Genet (2012) 3.58
Gain of function Naν1.7 mutations in idiopathic small fiber neuropathy. Ann Neurol (2011) 3.53
Sodium channels in normal and pathological pain. Annu Rev Neurosci (2010) 3.47
The Na(V)1.7 sodium channel: from molecule to man. Nat Rev Neurosci (2012) 2.71
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. J Physiol (2006) 2.62
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. Proc Natl Acad Sci U S A (2006) 2.61
Activated microglia contribute to the maintenance of chronic pain after spinal cord injury. J Neurosci (2006) 2.60
Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders. J Clin Invest (2007) 2.58
Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system. Pain (2012) 2.34
From genes to pain: Na v 1.7 and human pain disorders. Trends Neurosci (2007) 2.29
Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons. J Physiol (2003) 2.21
Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain (2004) 2.10
The roles of sodium channels in nociception: Implications for mechanisms of pain. Pain (2007) 2.06
Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes C-fiber nociceptors with broad action potentials and high Nav1.9 expression. J Neurosci (2006) 2.05
Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. Proc Natl Acad Sci U S A (2004) 1.99
Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy. Neurology (2006) 1.95
Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones. J Physiol (2005) 1.95
Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J Neurosci (2004) 1.93
NaN/Nav1.9: a sodium channel with unique properties. Trends Neurosci (2002) 1.93
Fibroblast growth factor homologous factor 2B: association with Nav1.6 and selective colocalization at nodes of Ranvier of dorsal root axons. J Neurosci (2004) 1.91
The presence and role of the tetrodotoxin-resistant sodium channel Na(v)1.9 (NaN) in nociceptive primary afferent neurons. J Neurosci (2002) 1.85
Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons. FEBS Lett (2005) 1.85
Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation. Brain (2009) 1.82
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons. Exp Neurol (2010) 1.78
Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury. J Neurosci (2003) 1.76
Intravenous administration of auto serum-expanded autologous mesenchymal stem cells in stroke. Brain (2011) 1.73
Modulation of the cardiac sodium channel Nav1.5 by fibroblast growth factor homologous factor 1B. J Biol Chem (2002) 1.64
GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones. J Physiol (2003) 1.62
A case of inherited erythromelalgia. Nat Clin Pract Neurol (2007) 1.60
A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. Ann Neurol (2012) 1.59
Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine. Ann Neurol (2007) 1.56
Early treatment suppresses the development of spike-wave epilepsy in a rat model. Epilepsia (2007) 1.53
FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels. Mol Cell Neurosci (2009) 1.51
Gain-of-function Nav1.8 mutations in painful neuropathy. Proc Natl Acad Sci U S A (2012) 1.50
Extracellular signal-regulated kinase-regulated microglia-neuron signaling by prostaglandin E2 contributes to pain after spinal cord injury. J Neurosci (2007) 1.49
Sporadic onset of erythermalgia: a gain-of-function mutation in Nav1.7. Ann Neurol (2006) 1.48
Nav1.5 sodium channels in macrophages in multiple sclerosis lesions. Mult Scler (2012) 1.45
Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury. J Comp Neurol (2003) 1.43
Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE. Brain (2003) 1.42
Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. J Neurosci (2006) 1.42
Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction. Brain Res Mol Brain Res (2002) 1.40
Familial pain syndromes from mutations of the NaV1.7 sodium channel. Ann N Y Acad Sci (2010) 1.40
International Union of Pharmacology. XXXIX. Compendium of voltage-gated ion channels: sodium channels. Pharmacol Rev (2003) 1.40
Differential modulation of sodium channel Na(v)1.6 by two members of the fibroblast growth factor homologous factor 2 subfamily. Eur J Neurosci (2006) 1.39
PGE2 increases the tetrodotoxin-resistant Nav1.9 sodium current in mouse DRG neurons via G-proteins. Brain Res (2004) 1.39
ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties. J Neurosci (2010) 1.38
Calmodulin binds to the C terminus of sodium channels Nav1.4 and Nav1.6 and differentially modulates their functional properties. J Neurosci (2003) 1.38
Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas. Ann Neurol (2008) 1.37
Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21. J Neurosci (2007) 1.36
Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis. Epilepsia (2008) 1.36
Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons. J Neurosci (2008) 1.35
A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity. J Physiol (2007) 1.35
Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminals. Mol Pain (2010) 1.33
Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neurons. J Neurosci (2003) 1.33
Voltage-gated sodium channels: therapeutic targets for pain. Pain Med (2009) 1.33
Transfection of rat or mouse neurons by biolistics or electroporation. Nat Protoc (2009) 1.32
Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability. Brain (2011) 1.32
Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in pain. Pain (2008) 1.32
Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable. Mol Pain (2008) 1.26
Abnormal sodium channel distribution in optic nerve axons in a model of inflammatory demyelination. Brain (2003) 1.25
A sodium channel gene SCN9A polymorphism that increases nociceptor excitability. Ann Neurol (2009) 1.25
Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury. J Neurosci (2004) 1.24
trkA is expressed in nociceptive neurons and influences electrophysiological properties via Nav1.8 expression in rapidly conducting nociceptors. J Neurosci (2005) 1.24
Voltage-gated sodium channel Nav1.6 is modulated by p38 mitogen-activated protein kinase. J Neurosci (2005) 1.23
Sodium channels contribute to microglia/macrophage activation and function in EAE and MS. Glia (2005) 1.22
Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade. Mol Pain (2008) 1.21
Changes of sodium channel expression in experimental painful diabetic neuropathy. Ann Neurol (2002) 1.20
Dysregulation of sodium channel expression in cortical neurons in a rodent model of absence epilepsy. Brain Res (2004) 1.20
Differential slow inactivation and use-dependent inhibition of Nav1.8 channels contribute to distinct firing properties in IB4+ and IB4- DRG neurons. J Neurophysiol (2006) 1.20
Small-fibre neuropathies--advances in diagnosis, pathophysiology and management. Nat Rev Neurol (2012) 1.19
A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia. Ann Neurol (2009) 1.18
Voltage-clamp and current-clamp recordings from mammalian DRG neurons. Nat Protoc (2009) 1.16
Pharmacological properties of neuronal TTX-resistant sodium channels and the role of a critical serine pore residue. Pflugers Arch (2005) 1.16
The ataxia3 mutation in the N-terminal cytoplasmic domain of sodium channel Na(v)1.6 disrupts intracellular trafficking. J Neurosci (2009) 1.16
Expression of the voltage-gated sodium channel NaV1.5 in the macrophage late endosome regulates endosomal acidification. J Immunol (2007) 1.16
Neuropathic pain memory is maintained by Rac1-regulated dendritic spine remodeling after spinal cord injury. J Neurosci (2008) 1.15
Changes in electrophysiological properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury. Brain (2005) 1.15
Long-term protection of central axons with phenytoin in monophasic and chronic-relapsing EAE. Brain (2006) 1.15
Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating. J Biol Chem (2006) 1.15
An ankyrinG-binding motif is necessary and sufficient for targeting Nav1.6 sodium channels to axon initial segments and nodes of Ranvier. J Neurosci (2012) 1.13
Novel SCN1A mutation in a proband with malignant migrating partial seizures of infancy. Arch Neurol (2011) 1.12
Regulation of podosome formation in macrophages by a splice variant of the sodium channel SCN8A. J Biol Chem (2009) 1.12
Neurobiology: a channel sets the gain on pain. Nature (2006) 1.10
Neurological channelopathies: new insights into disease mechanisms and ion channel function. J Physiol (2010) 1.09
Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7. Mol Pain (2011) 1.09
Upregulation of persistent and ramp sodium current in dorsal horn neurons after spinal cord injury. Exp Brain Res (2006) 1.09
Mesenchymal stem cells: therapeutic outlook for stroke. Trends Mol Med (2012) 1.08
Neuropathic pain in diabetes--evidence for a central mechanism. Nat Rev Neurol (2010) 1.08
Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons. Eur J Neurosci (2005) 1.07
Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn. Mol Pain (2012) 1.07
Protection of corticospinal tract neurons after dorsal spinal cord transection and engraftment of olfactory ensheathing cells. Glia (2006) 1.07
Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivo. J Neurophysiol (2003) 1.06
Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice. Neurobiol Aging (2005) 1.05
Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons. J Neurosci (2013) 1.04
Nitric oxide blocks fast, slow, and persistent Na+ channels in C-type DRG neurons by S-nitrosylation. J Neurophysiol (2002) 1.04
Alterations in burst firing of thalamic VPL neurons and reversal by Na(v)1.3 antisense after spinal cord injury. J Neurophysiol (2006) 1.04
Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia. Brain (2010) 1.04
Disruption of cAMP and prostaglandin E2 transport by multidrug resistance protein 4 deficiency alters cAMP-mediated signaling and nociceptive response. Mol Pharmacol (2007) 1.03