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The Role of Voltage-Gated Sodium Channels in Pain Signaling

Physiological reviews, 2019-04, Vol.99 (2), p.1079-1151

2019

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Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics

Annual review of neuroscience, 2019-07, Vol.42 (1), p.87-106

2019

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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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Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

Scientific reports, 2018-03, Vol.8 (1), p.1-17, Article 3845

2018

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A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia

Molecular medicine (Cambridge, Mass.), 2016, Vol.22 (1), p.338-348

2016

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Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp

The Journal of neuroscience, 2019-01, Vol.39 (3), p.382-392

2019

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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

American journal of human genetics, 2012-03, Vol.90 (3), p.502-510

2012

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Genetic, electrophysiological, and pathological studies on patients with SCN9A‐related pain disorders

Journal of the peripheral nervous system, 2023-12, Vol.28 (4), p.597-607

2023

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Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones

The Journal of physiology, 2005-05, Vol.564 (3), p.803-815

2005

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Expression of Nav1.7 in DRG Neurons Extends from Peripheral Terminals in the Skin to Central Preterminal Branches and Terminals in the Dorsal Horn

Molecular pain, 2012-11, Vol.8 (1), p.82-82

2012

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Gain-of-function Naᵥ1.8 mutations in painful neuropathy

Proceedings of the National Academy of Sciences - PNAS, 2012-11, Vol.109 (47), p.19444-19449

2012

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Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

Brain (London, England : 1878), 2014-06, Vol.137 (6), p.1627-1642

2014

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A TRPM7 mutation linked to familial trigeminal neuralgia: Omega current and hyperexcitability of trigeminal ganglion neurons

Proceedings of the National Academy of Sciences - PNAS, 2022-09, Vol.119 (38), p.e2119630119-e2119630119

2022

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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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Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons

The Journal of neuroscience, 2013-08, Vol.33 (35), p.14087-14097

2013

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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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NaV1.6 regulates excitability of mechanosensitive sensory neurons

The Journal of physiology, 2019-07, Vol.597 (14), p.3751-3768

2019

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Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

Cell reports (Cambridge), 2024-02, Vol.43 (2), p.113685-113685, Article 113685

2024

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Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

Pain (Amsterdam), 2020-04, Vol.161 (4), p.831-841

2020

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A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons

Proceedings of the National Academy of Sciences - PNAS, 2006-05, Vol.103 (21), p.8245-8250

2006

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A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Neurobiology of disease, 2014-09, Vol.69, p.117-123

2014

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Translational pain research: Lessons from genetics and genomics

Science translational medicine, 2014-08, Vol.6 (249), p.249sr4

2014

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A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

Frontiers in neuroscience, 2019-09, Vol.13, p.918-918

2019

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Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development

PloS one, 2015-04, Vol.10 (4), p.e0124397-e0124397

2015

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Familial gain-of-function Nav1.9 mutation in a painful channelopathy

Journal of neurology, neurosurgery and psychiatry, 2017-03, Vol.88 (3), p.233-240

2017

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The Role of Voltage-Gated Sodium Channels in Pain Signaling

Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics

Sodium Channels in Normal and Pathological Pain

Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia

Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp

De Novo Pathogenic SCN8A Mutation Identified by Whole-Genome Sequencing of a Family Quartet Affected by Infantile Epileptic Encephalopathy and SUDEP

Genetic, electrophysiological, and pathological studies on patients with SCN9A‐related pain disorders

Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones

Expression of Nav1.7 in DRG Neurons Extends from Peripheral Terminals in the Skin to Central Preterminal Branches and Terminals in the Dorsal Horn

Gain-of-function Naᵥ1.8 mutations in painful neuropathy

Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

A TRPM7 mutation linked to familial trigeminal neuralgia: Omega current and hyperexcitability of trigeminal ganglion neurons

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

Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons

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

NaV1.6 regulates excitability of mechanosensitive sensory neurons

Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons

A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Translational pain research: Lessons from genetics and genomics

A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development

Familial gain-of-function Nav1.9 mutation in a painful channelopathy

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