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Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons

Brain (London, England : 1878), 2005-08, Vol.128 (8), p.1847-1854

2005

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The molecular genetic architecture of attention deficit hyperactivity disorder

Molecular psychiatry, 2015-03, Vol.20 (3), p.289-297

2015

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Persistent TTX-Resistant Na+ Current Affects Resting Potential and Response to Depolarization in Simulated Spinal Sensory Neurons

Journal of neurophysiology, 2001-09, Vol.86 (3), p.1351-1364

2001

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Sodium Channels and Pain

Proceedings of the National Academy of Sciences - PNAS, 1999-07, Vol.96 (14), p.7635-7639

1999

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A Novel Persistent Tetrodotoxin-Resistant Sodium Current In SNS-Null And Wild-Type Small Primary Sensory Neurons

The Journal of neuroscience, 1999-12, Vol.19 (24), p.43-RC43

1999

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Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons

The Journal of physiology, 2003-09, Vol.551 (3), p.741-750

2003

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Upregulation of a Silent Sodium Channel After Peripheral, but not Central, Nerve Injury in DRG Neurons

Journal of neurophysiology, 1999-11, Vol.82 (5), p.2776-2785

1999

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Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons

Journal of neurophysiology, 2001-08, Vol.86 (2), p.629

2001

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A gain-of-function mutation in the sodium channel gene Scn2a results in seizures and behavioral abnormalities

Neuroscience, 2001-01, Vol.102 (2), p.307-317

2001

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Changes in Expression of Two Tetrodotoxin-Resistant Sodium Channels and Their Currents in Dorsal Root Ganglion Neurons after Sciatic Nerve Injury But Not Rhizotomy

The Journal of neuroscience, 2000-10, Vol.20 (19), p.7279-7289

2000

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Nitric Oxide Blocks Fast, Slow, and Persistent Na+ Channels in C-Type DRG Neurons by S-Nitrosylation

Journal of neurophysiology, 2002-02, Vol.87 (2), p.761-775

2002

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Vasodilatation in the rat dorsal hindpaw induced by activation of sensory neurons is reduced by paclitaxel

Neurotoxicology (Park Forest South), 2011-01, Vol.32 (1), p.140-149

2011

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Glial-Derived Neurotrophic Factor Upregulates Expression of Functional SNS and NaN Sodium Channels and Their Currents in Axotomized Dorsal Root Ganglion Neurons

The Journal of neuroscience, 2000-12, Vol.20 (23), p.8754-8761

2000

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Nav1.3 Sodium Channels: Rapid Repriming and Slow Closed-State Inactivation Display Quantitative Differences after Expression in a Mammalian Cell Line and in Spinal Sensory Neurons

The Journal of neuroscience, 2001-08, Vol.21 (16), p.5952-5961

2001

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Sodium Channels in Normal and Pathological Pain

Annual review of neuroscience, 2010-01, Vol.33 (1), p.325-347

2010

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Downregulation of Tetrodotoxin-Resistant Sodium Currents and Upregulation of a Rapidly Repriming Tetrodotoxin-Sensitive Sodium Current in Small Spinal Sensory Neurons after Nerve Injury

The Journal of neuroscience, 1997-05, Vol.17 (10), p.3503-3514

1997

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Impairment of slow inactivation as a common mechanism for periodic paralysis in DIIS4-S5

Neurology, 2002-04, Vol.58 (8), p.1266

2002

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SNS Na+ channel expression increases in dorsal root ganglion neurons in the carrageenan inflammatory pain model

Neuroreport, 1998-04, Vol.9 (6), p.967-972

1998

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Slow Closed-State Inactivation: A Novel Mechanism Underlying Ramp Currents in Cells Expressing the hNE/PN1 Sodium Channel

The Journal of neuroscience, 1998-12, Vol.18 (23), p.9607-9619

1998

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Rescue of alpha -SNS Sodium Channel Expression in Small Dorsal Root Ganglion Neurons After Axotomy by Nerve Growth Factor In Vivo

Journal of neurophysiology, 1998-05, Vol.79 (5), p.2668-2676

1998

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Two tetrodotoxin-resistant sodium channels in human dorsal root ganglion neurons

FEBS letters, 1999-11, Vol.462 (1), p.117-120

1999

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Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain

Pain (Amsterdam), 1999-12, Vol.83 (3), p.591-600

1999

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Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain

Muscle & nerve, 1999-09, Vol.22 (9), p.1177-1187

1999

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Unusual Voltage-Gated Sodium Currents as Targets for Pain

Current topics in membranes, 2016, Vol.78, p.599

2016

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alpha -SNS Produces the Slow TTX-Resistant Sodium Current in Large Cutaneous Afferent DRG Neurons

Journal of neurophysiology, 2000-08, Vol.84 (2), p.710-718

2000

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Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons

The molecular genetic architecture of attention deficit hyperactivity disorder

Persistent TTX-Resistant Na+ Current Affects Resting Potential and Response to Depolarization in Simulated Spinal Sensory Neurons

Sodium Channels and Pain

A Novel Persistent Tetrodotoxin-Resistant Sodium Current In SNS-Null And Wild-Type Small Primary Sensory Neurons

Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons

Upregulation of a Silent Sodium Channel After Peripheral, but not Central, Nerve Injury in DRG Neurons

Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons

A gain-of-function mutation in the sodium channel gene Scn2a results in seizures and behavioral abnormalities

Changes in Expression of Two Tetrodotoxin-Resistant Sodium Channels and Their Currents in Dorsal Root Ganglion Neurons after Sciatic Nerve Injury But Not Rhizotomy

Nitric Oxide Blocks Fast, Slow, and Persistent Na+ Channels in C-Type DRG Neurons by S-Nitrosylation

Vasodilatation in the rat dorsal hindpaw induced by activation of sensory neurons is reduced by paclitaxel

Glial-Derived Neurotrophic Factor Upregulates Expression of Functional SNS and NaN Sodium Channels and Their Currents in Axotomized Dorsal Root Ganglion Neurons

Nav1.3 Sodium Channels: Rapid Repriming and Slow Closed-State Inactivation Display Quantitative Differences after Expression in a Mammalian Cell Line and in Spinal Sensory Neurons

Sodium Channels in Normal and Pathological Pain

Downregulation of Tetrodotoxin-Resistant Sodium Currents and Upregulation of a Rapidly Repriming Tetrodotoxin-Sensitive Sodium Current in Small Spinal Sensory Neurons after Nerve Injury

Impairment of slow inactivation as a common mechanism for periodic paralysis in DIIS4-S5

SNS Na+ channel expression increases in dorsal root ganglion neurons in the carrageenan inflammatory pain model

Slow Closed-State Inactivation: A Novel Mechanism Underlying Ramp Currents in Cells Expressing the hNE/PN1 Sodium Channel

Rescue of alpha -SNS Sodium Channel Expression in Small Dorsal Root Ganglion Neurons After Axotomy by Nerve Growth Factor In Vivo

Two tetrodotoxin-resistant sodium channels in human dorsal root ganglion neurons

Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain

Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain

Unusual Voltage-Gated Sodium Currents as Targets for Pain

alpha -SNS Produces the Slow TTX-Resistant Sodium Current in Large Cutaneous Afferent DRG Neurons

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