Nature Search

A case of inherited erythromelalgia

Steven P Novella
Fuki M Hisama
Stephen G Waxman
Reviews01 Apr 2007
Nature Clinical Practice Neurology

Volume: 3, P: 229-234
Paroxysmal extreme pain disorder: a molecular lesion of peripheral neurons

Choi et al. describe the case of a 3 month-old infant who, on the second day of life, had begun to experience painful paroxysmal events starting with tonic contraction of the whole body followed by erythematous harlequin-type color changes. The patient was diagnosed as having paroxysmal extreme pain disorder. The condition was attributed to a mutation in the SCN9A gene, which encodes the voltage-gated sodium channel Na_V1.7.

Jin-Sung Choi
Franck Boralevi
Stephen G. Waxman
Reviews16 Nov 2010
Nature Reviews Neurology

Volume: 7, P: 51-55
Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Theodore R Cummins
Anthony M Rush
Stephen G Waxman
Protocols09 Jul 2009
Nature Protocols

Volume: 4, P: 1103-1112
Real-time imaging of axonal membrane protein life cycles

Conjugation of self-labeling enzymatic tags to axonal membrane proteins enables studying the dynamics of their trafficking, cellular localization and fate.

Sidharth Tyagi
Grant P. Higerd-Rusli
Sulayman D. Dib-Hajj
Protocols03 Jun 2024
Nature Protocols

Volume: 19, P: 2771-2802
Voltage-gated sodium channels in excitable cells as drug targets

The family of voltage-gated sodium channels (Na_Vs) are key mediators of electrical signals in excitable cells. In their broad Review, Waxman and colleagues discuss the potential to target Na_Vs in neurons, cardiac and skeletal muscle cells for the treatment of various neurological and muscular disorders.

Matthew Alsaloum
Sulayman D. Dib-Hajj
Stephen G. Waxman
Reviews03 Feb 2025
Nature Reviews Drug Discovery

Volume: 24, P: 358-378
Na_V1.9: a sodium channel linked to human pain

Emerging evidence suggests a role for the voltage-gated sodium channel Na_V1.9 in pain. In this Progress article, Dib-Hajj, Black and Waxman analyse the findings from three studies that report mutations in the gene encoding Na_V1.9 in pain disorders, and suggest that Na_V1.9 may be a potential therapeutic target for pain.

Sulayman D. Dib-Hajj
Joel A. Black
Stephen G. Waxman
Reviews05 Aug 2015
Nature Reviews Neuroscience

Volume: 16, P: 511-519
Conditional knockout of Na_V1.6 in adult mice ameliorates neuropathic pain

Lubin Chen
Jianying Huang
Sulayman D. Dib-Hajj
ResearchOpen Access01 Mar 2018
Scientific Reports

Volume: 8, P: 1-17
Sculpting excitable membranes: voltage-gated ion channel delivery and distribution

Neuronal function depends upon the domain-specific localization of membrane ion channels. Tyagi et al. describe our current understanding of the mechanisms that regulate ion channel delivery to specific neuronal compartments, with a focus on the distribution of voltage-gated sodium channels in peripheral sensory axons.

Sidharth Tyagi
Grant P. Higerd-Rusli
Sulayman D. Dib-Hajj
Reviews02 Apr 2025
Nature Reviews Neuroscience

Volume: 26, P: 313-332
Pain-causing stinging nettle toxins target TMEM233 to modulate Na_V1.7 function

Voltage-gated sodium channels function as multiprotein signaling complexes. Here, authors show that the dispanin TMEM233 is essential for activity of stinging nettle toxins and that co-expression of TMEM233 modulates the gating properties of Na_V1.7.

Sina Jami
Jennifer R. Deuis
Irina Vetter
ResearchOpen Access28 Apr 2023
Nature Communications

Volume: 14, P: 1-16
Transfection of rat or mouse neurons by biolistics or electroporation

Sulayman D Dib-Hajj
Jin Sung Choi
Stephen G Waxman
Protocols09 Jul 2009
Nature Protocols

Volume: 4, P: 1118-1127
Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na_v1.7 mutant channel

Mutations of the Na_V1.7 voltage-gated sodium channel are implicated in abnormal pain signal transduction. Yang and colleagues perform structural modeling, mutant cycle analysis and electrophysiology on specific mutants and find that they can accurately predict their response profiles to channel blockers.

Yang Yang
Sulayman D. Dib-Hajj
Stephen G. Waxman
Research13 Nov 2012
Nature Communications

Volume: 3, P: 1-12
The Na_V1.7 sodium channel: from molecule to man

Mutations inSCN9A, which encodes the voltage-gated sodium channel Na_V1.7, can lead to severe neuropathic pain in humans. In this Review, Waxman and colleagues examine the mechanistic basis of Na_V1.7-linked pain and explore strategies for targeting this channel in pain therapy.

Sulayman D. Dib-Hajj
Yang Yang
Stephen G. Waxman
Reviews12 Dec 2012
Nature Reviews Neuroscience

Volume: 14, P: 49-62
High-throughput multiplex voltage-clamp/current-clamp evaluation of acutely isolated neurons

This Protocol describes an automated high-throughput patch-clamp approach that enables the simultaneous and unbiased analysis of acutely dissociated neurons in their native state, with diverse applications ranging from the assessment of neuronal biophysics to drug development.

Mohammad-Reza Ghovanloo
Sidharth Tyagi
Stephen G. Waxman
Protocols13 Jun 2025
Nature Protocols

P: 1-26
Correction: Corrigendum: Pharmacological characterisation of the highly Na_V1.7 selective spider venom peptide Pn3a

Jennifer R. Deuis
Zoltan Dekan
Irina Vetter
Amendments and CorrectionsOpen Access26 May 2017
Scientific Reports

Volume: 7, P: 1
Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Na_v1.7 mutation that massively hyperpolarizes activation

Jianying Huang
Malgorzata A. Mis
Stephen G. Waxman
ResearchOpen Access29 Jan 2018
Scientific Reports

Volume: 8, P: 1-13
Maximizing treatment efficacy through patient stratification in neuropathic pain trials

Despite substantial research advances, treatment of neuropathic pain remains inadequate and responses to treatment are highly variable. In this Perspective, the authors argue that rational stratification of patients with neuropathic pain will aid identification of subgroups of patients who will benefit most from a given treatment.

Ralf Baron
Anthony H. Dickenson
David L. Bennett
Reviews18 Nov 2022
Nature Reviews Neurology

Volume: 19, P: 53-64
Functionally-selective inhibition of threshold sodium currents and excitability in dorsal root ganglion neurons by cannabinol

Cannabinol (CBN) is a promising compound that is suggested as an analgesic. Using electrophysiological techniques, this study determined that CBN inhibits the sodium currents associated with pain signaling, with potential application for neuropathic pain.

Mohammad-Reza Ghovanloo
Philip R. Effraim
Stephen G. Waxman
ResearchOpen Access23 Jan 2024
Communications Biology

Volume: 7, P: 1-17
Loss-of-function mutations of SCN10A encoding Na_V1.8 α subunit of voltage-gated sodium channel in patients with human kidney stone disease

Choochai Nettuwakul
Oranud Praditsap
Pa-thai Yenchitsomanus
ResearchOpen Access11 Jul 2018
Scientific Reports

Volume: 8, P: 1-12
Pharmacological characterisation of the highly Na_V1.7 selective spider venom peptide Pn3a

Jennifer R. Deuis
Zoltan Dekan
Irina Vetter
ResearchOpen Access20 Jan 2017
Scientific Reports

Volume: 7, P: 1-19

Search

A case of inherited erythromelalgia

Paroxysmal extreme pain disorder: a molecular lesion of peripheral neurons

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Real-time imaging of axonal membrane protein life cycles

Voltage-gated sodium channels in excitable cells as drug targets

Na_V1.9: a sodium channel linked to human pain

Conditional knockout of Na_V1.6 in adult mice ameliorates neuropathic pain

Sculpting excitable membranes: voltage-gated ion channel delivery and distribution

Pain-causing stinging nettle toxins target TMEM233 to modulate Na_V1.7 function

Transfection of rat or mouse neurons by biolistics or electroporation

Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na_v1.7 mutant channel

The Na_V1.7 sodium channel: from molecule to man

High-throughput multiplex voltage-clamp/current-clamp evaluation of acutely isolated neurons

Correction: Corrigendum: Pharmacological characterisation of the highly Na_V1.7 selective spider venom peptide Pn3a

Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Na_v1.7 mutation that massively hyperpolarizes activation

Maximizing treatment efficacy through patient stratification in neuropathic pain trials

Functionally-selective inhibition of threshold sodium currents and excitability in dorsal root ganglion neurons by cannabinol

Loss-of-function mutations of SCN10A encoding Na_V1.8 α subunit of voltage-gated sodium channel in patients with human kidney stone disease

Pharmacological characterisation of the highly Na_V1.7 selective spider venom peptide Pn3a

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