Published in Brain Res on March 12, 2004
Reduced cortical inhibition in a mouse model of familial childhood absence epilepsy. Proc Natl Acad Sci U S A (2007) 1.82
Molecular targets for antiepileptic drug development. Neurotherapeutics (2007) 1.78
Early treatment suppresses the development of spike-wave epilepsy in a rat model. Epilepsia (2007) 1.53
Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice. Hum Mol Genet (2009) 1.45
Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis. Epilepsia (2008) 1.36
Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4. Hum Mol Genet (2008) 1.36
Inherited cortical HCN1 channel loss amplifies dendritic calcium electrogenesis and burst firing in a rat absence epilepsy model. J Physiol (2006) 1.34
Consciousness and epilepsy: why are patients with absence seizures absent? Prog Brain Res (2005) 1.34
De novo gain-of-function and loss-of-function mutations of SCN8A in patients with intellectual disabilities and epilepsy. J Med Genet (2015) 1.17
Where fMRI and electrophysiology agree to disagree: corticothalamic and striatal activity patterns in the WAG/Rij rat. J Neurosci (2011) 1.16
Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy. J Physiol (2006) 1.15
Single-channel properties of human NaV1.1 and mechanism of channel dysfunction in SCN1A-associated epilepsy. J Gen Physiol (2006) 1.14
DTI abnormalities in anterior corpus callosum of rats with spike-wave epilepsy. Neuroimage (2009) 1.13
Absence seizures: individual patterns revealed by EEG-fMRI. Epilepsia (2010) 1.11
Focal BOLD fMRI changes in bicuculline-induced tonic-clonic seizures in the rat. Neuroimage (2010) 1.02
Evidence for a role of Nav1.6 in facilitating increases in neuronal hyperexcitability during epileptogenesis. J Neurophysiol (2013) 1.00
In silico docking and electrophysiological characterization of lacosamide binding sites on collapsin response mediator protein-2 identifies a pocket important in modulating sodium channel slow inactivation. J Biol Chem (2010) 0.98
Dynamics of networks during absence seizure's on- and offset in rodents and man. Front Physiol (2015) 0.89
Spatiotemporal dynamics of optogenetically induced and spontaneous seizure transitions in primary generalized epilepsy. J Neurophysiol (2014) 0.89
Neuroimaging biomarkers of epileptogenesis. Neurosci Lett (2011) 0.89
Anti-epileptogenesis: Electrophysiology, diffusion tensor imaging and behavior in a genetic absence model. Neurobiol Dis (2013) 0.88
Cellular and network mechanisms of genetically-determined absence seizures. Thalamus Relat Syst (2007) 0.86
Is epilepsy a preventable disorder? New evidence from animal models. Neuroscientist (2010) 0.86
Integrative properties and transfer function of cortical neurons initiating absence seizures in a rat genetic model. J Physiol (2016) 0.85
Functional neuroimaging of spike-wave seizures. Methods Mol Biol (2009) 0.85
Molecular identity of axonal sodium channels in human cortical pyramidal cells. Front Cell Neurosci (2014) 0.84
Development of spike-wave seizures in C3H/HeJ mice. Epilepsy Res (2009) 0.81
Effect of systemic and intracortical administration of phenytoin in two genetic models of absence epilepsy. Br J Pharmacol (2006) 0.80
Diminished presynaptic GABA(B) receptor function in the neocortex of a genetic model of absence epilepsy. Neurosignals (2009) 0.78
Focal interictal epileptiform discharges in idiopathic generalized epilepsy. Neurol Sci (2016) 0.75
Unilateral and Bilateral Cortical Resection: Effects on Spike-Wave Discharges in a Genetic Absence Epilepsy Model. PLoS One (2015) 0.75
International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels. Pharmacol Rev (2005) 5.40
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
Cerebral energetics and spiking frequency: the neurophysiological basis of fMRI. Proc Natl Acad Sci U S A (2002) 2.28
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
The role of subcortical structures in human epilepsy. Epilepsy Behav (2002) 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
Dynamic time course of typical childhood absence seizures: EEG, behavior, and functional magnetic resonance imaging. J Neurosci (2010) 1.89
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
Negative BOLD with large increases in neuronal activity. Cereb Cortex (2007) 1.71
Remote effects of focal hippocampal seizures on the rat neocortex. J Neurosci (2008) 1.69
Energetics of neuronal signaling and fMRI activity. Proc Natl Acad Sci U S A (2007) 1.65
Modulation of the cardiac sodium channel Nav1.5 by fibroblast growth factor homologous factor 1B. J Biol Chem (2002) 1.64
Impaired consciousness in partial seizures is bimodally distributed. Neurology (2014) 1.63
Redundancy and synergy of neuronal ensembles in motor cortex. J Neurosci (2005) 1.62
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
Comparison of statistical parametric mapping and SPECT difference imaging in patients with temporal lobe epilepsy. Epilepsia (2002) 1.57
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
Simultaneous EEG, fMRI, and behavior in typical childhood absence seizures. Epilepsia (2010) 1.44
Impaired consciousness in temporal lobe seizures: role of cortical slow activity. Brain (2010) 1.44
Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury. J Comp Neurol (2003) 1.43
Cortical deactivation induced by subcortical network dysfunction in limbic seizures. J Neurosci (2009) 1.42
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
Localizing value of ictal-interictal SPECT analyzed by SPM (ISAS). Epilepsia (2005) 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
Dynamic fMRI and EEG recordings during spike-wave seizures and generalized tonic-clonic seizures in WAG/Rij rats. J Cereb Blood Flow Metab (2004) 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
Cerebral perfusion changes in older delirious patients using 99mTc HMPAO SPECT. J Gerontol A Biol Sci Med Sci (2006) 1.32
Transfection of rat or mouse neurons by biolistics or electroporation. Nat Protoc (2009) 1.32
Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in pain. Pain (2008) 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
LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology. Mol Cell Neurosci (2009) 1.32
Impaired attention and network connectivity in childhood absence epilepsy. Neuroimage (2011) 1.27
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
Relative changes in cerebral blood flow and neuronal activity in local microdomains during generalized seizures. J Cereb Blood Flow Metab (2004) 1.22
Sodium channels contribute to microglia/macrophage activation and function in EAE and MS. Glia (2005) 1.22
Oxidative neuroenergetics in event-related paradigms. J Neurosci (2009) 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
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
The brain in diabetes: molecular changes in neurons and their implications for end-organ damage. Lancet Neurol (2003) 1.18
A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia. Ann Neurol (2009) 1.18
Current aproach to cancer pain management: Availability and implications of different treatment options. Ther Clin Risk Manag (2007) 1.17
Voltage-clamp and current-clamp recordings from mammalian DRG neurons. Nat Protoc (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
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
Where fMRI and electrophysiology agree to disagree: corticothalamic and striatal activity patterns in the WAG/Rij rat. J Neurosci (2011) 1.16