Brian S. Tanaka

Correction of sodium channel mutations in sensory neurons reverses aberrant properties

Jaehoon Shim, Brian S. Tanaka, Daniel G. Taub, Malgorzata A. Mis et autres

Inherited erythromelalgia, small fibre neuropathy and paroxysmal extreme pain disorder are caused by gain-of-function mutations in the voltage-gated sodium channel Nav1.7. It remains unknown how different mutations in the same channel enhancing electrogenesis in sensory neurons results in such distinct disease presentations. …

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Lacosamide Inhibition of NaV1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore

Julie I. R. Labau, Matthew Alsaloum, Mark Estación, Brian S. Tanaka et autres

Lacosamide, developed as an anti-epileptic drug, has been used for the treatment of pain. Unlike typical anticonvulsants and local anesthetics which enhance fast-inactivation and bind within the pore of sodium channels, lacosamide enhances slow-inactivation of these channels, suggesting different binding mechanisms and …

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KCNQ variants and pain modulation: a missense variant in Kv7.3 contributes to pain resilience

Jun‐Hui Yuan, Mark Estación, Malgorzata A. Mis, Brian S. Tanaka et autres

Abstract There is a pressing need for understanding of factors that confer resilience to pain. Gain-of-function mutations in sodium channel Nav1.7 produce hyperexcitability of dorsal root ganglion neurons underlying inherited erythromelalgia, a human genetic model of neuropathic pain. While most individuals with …

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Pharmacological activity and NMR solution structure of the leech peptide HSTX-I

Kirsten L. McMahon, Bryan Tay, Jennifer R. Deuis, Brian S. Tanaka et autres

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Differential effect of lacosamide on Nav1.7 variants from responsive and non-responsive patients with small fibre neuropathy

Julie I. R. Labau, Mark Estación, Brian S. Tanaka, Bianca T. A. de Greef et autres

Small fibre neuropathy is a common pain disorder, which in many cases fails to respond to treatment with existing medications. Gain-of-function mutations of voltage-gated sodium channel Nav1.7 underlie dorsal root ganglion neuronal hyperexcitability and pain in a subset of patients with small …

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

Matteo Urru, Mirko Muzzi, Elisabetta Coppi, Giuseppe Ranieri et autres

Selective targeting of sodium channel subtypes Nav1.7, Nav1.8, and Nav1.9, preferentially expressed by peripheral nociceptors, represents a unique opportunity to develop analgesics devoid of central side effects. Several compounds that target Nav1.7 and Nav1.8 with different degrees of selectivity have been developed …

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Building sensory axons: Delivery and distribution of Na V 1.7 channels and effects of inflammatory mediators

Elizabeth J. Akin, Grant P. Higerd‐Rusli, Malgorzata A. Mis, Brian S. Tanaka et autres

Sodium channel Na V 1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and functional studies. However, little is known about Na V 1.7 trafficking or membrane distribution along sensory axons, which can be a …

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NaV1.6 regulates excitability of mechanosensitive sensory neurons

Mathilde R. Israel, Brian S. Tanaka, Joel Castro, Panumart Thongyoo et autres

Key points Voltage‐gated sodium channels are critical for peripheral sensory neuron transduction and have been implicated in a number of painful and painless disorders. The β‐scorpion toxin, Cn2, is selective for NaV1.6 in dorsal root ganglion neurons. NaV1.6 plays an essential role …

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Restoration of brain circulation and cellular functions hours post-mortem

Zvonimir Vrselja, Stefano G. Daniele, John Silbereis, Francesca Talpo et autres

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

Malgorzata A. Mis, Yang Yang, Brian S. Tanaka, Carolina Gomis‐Pérez et autres

Pain is a complex process that involves both detection in the peripheral nervous system and perception in the CNS. Individual-to-individual differences in pain are well documented, but not well understood. Here we capitalized on inherited erythromelalgia (IEM), a well characterized human genetic …

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Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation

Jianying Huang, Malgorzata A. Mis, Brian S. Tanaka, Talia Adi et autres

Abstract Sodium channel Nav1.7 plays a central role in pain-signaling: gain-of-function Nav1.7 mutations usually cause severe pain and loss-of-function mutations produce insensitivity to pain. The Nav1.7 I234T gain-of-function mutation, however, is linked to a dual clinical presentation of episodic pain, together with …

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Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development

Brian S. Tanaka, Phuong T. Nguyen, Eray Yihui Zhou, Yong Yang et autres

Dominant mutations in voltage-gated sodium channel Na V 1.7 cause inherited erythromelalgia, a debilitating pain disorder characterized by severe burning pain and redness of the distal extremities. Na V 1.7 is preferentially expressed within peripheral sensory and sympathetic neurons. Here, we describe …

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