Deletion mutation of sodium channel NaV1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability

A novel slow-inactivation-specific ion channel modulator attenuates neuropathic pain

(2011) Michael E. Hildebrand et al.   PAIN

Sodium Channels in Normal and Pathological Pain

(2010) Sulayman D. Dib-Hajj et al.   Annual Review of Neuroscience

Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia

(2010) Jin-Sung Choi et al.   BRAIN

Lacosamide: An Adjunctive Agent for Partial-Onset Seizures and Potential Therapy for Neuropathic Pain

(2009) Jacklyn A Harris et al.   ANNALS OF PHARMACOTHERAPY

Early- and late-onset inherited erythromelalgia: genotype–phenotype correlation

(2009) Chongyang Han et al.   BRAIN

Transfection of rat or mouse neurons by biolistics or electroporation

(2009) Sulayman D Dib-Hajj et al.   Nature Protocols

Models of the Structure and Gating Mechanisms of the Pore Domain of the NaChBac Ion Channel

(2008) Yinon Shafrir et al.   BIOPHYSICAL JOURNAL

NaV1.7 Gain-of-Function Mutations as a Continuum: A1632E Displays Physiological Changes Associated with Erythromelalgia and Paroxysmal Extreme Pain Disorder Mutations and Produces Symptoms of Both Disorders

(2008) M. Estacion et al.   JOURNAL OF NEUROSCIENCE

Differential Block of Sensory Neuronal Voltage-Gated Sodium Channels by Lacosamide [(2R)-2-(Acetylamino)-N-benzyl-3-methoxypropanamide], Lidocaine, and Carbamazepine

(2008) P. L. Sheets et al.   JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS

Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation

(2008) Brian W. Jarecki et al.   JOURNAL OF PHYSIOLOGY-LONDON

Mutation I136V Alters Electrophysiological Properties of the NaV1.7 Channel in a Family with Onset of Erythromelalgia in the Second Decade

(2008) Xiaoyang Cheng et al.   Molecular Pain