bioRxivNeurosciencePreprint
Biophysical Characterization of the human Nav1.9 sodium channel in trigeminal ganglia and dorsal root ganglia neurons
Yu Patrick ShiiD, Tamara Cotta, Ian J. Orozco, Fanny Chen, Yannick Miron, Richard Kondo, Mark L. ChapmaniD, Douglas S. KrafteiD, Andre GhettiiD, Kevin P. Carlin
Abstract
In human dorsal root ganglia (DRG), and trigeminal (TG) neurons, the various voltage-gated sodium channel (Nav) isoforms play critical roles in the firing of action potentials, which drive electrical impulses that encode somatosensations including, itch, and pain. The SCN11A gene encodes the tetrodotoxin (TTX)-resistant voltage-gated sodium channel Nav1.9, characterized by unique gating properties. Unlike other isoforms, the Nav1.9 channel activates and inactivates slowly and has a hyperpolarized voltage-dependence of activation and depolarized voltage-dependence of inactivation. This leads to a large window current that has been suggested to function as a regulator of the resting membrane potential of neurons. Mutations in Nav1.9 channels lead to congenital insensitivity to pain (gain-of-function) or familial episodic pain syndrome (loss-of-function) suggesting the channel is a critical mediator of pain. Despite its relevance in pain pathophysiology, most existing data relies on rodent models or heterologous expression systems, leaving the specific pharmacology and biophysical behavior of these channels in human primary neurons largely unknown. In this study, we pharmacologically isolated and characterized native Nav1.9 channel currents in human DRG and TG neurons to compare their biophysical profiles. Our findings reveal significant kinetic and voltage-dependent differences between the two populations. Specifically, Nav1.9 channels in TG neurons exhibit a right-shifted steady-state inactivation curve, a larger window current, and faster activation kinetics compared to those in DRG neurons. In addition, conditions that simulate inflammatory states in-vivo greatly potentiates the Nav1.9 currents consistent with similar observations in rodent models. By detailing these distinct biophysical properties, this research offers crucial insights into Nav1.9 channel function relevant for drug discovery efforts aimed at developing analgesics for both acute and chronic pain.
- organism: human
- assay: electronic health records
- research focus: drug response / drug discovery
- approach: experimental assay
- Citations
- 0
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Modulation of human dorsal root ganglion neuron excitability by Nav1.7 inhibition
Akie Fujita, Sooyeon Jo, … Bruce P. Bean·eLifePeer-reviewed·Oct 23, 2026
- Sodium channels expressed in nociceptors contribute distinctly to action potential subthreshold phase, upstroke and shoulder
P. A. Köster, E. Leipold, … A. Lampert·bioRxiv·Sep 3, 2023
- Intranasal CRMP2-Ubc9 Inhibitor Regulates NaV1.7 to Alleviate Trigeminal Neuropathic Pain
Santiago Loya‐López, Heather N. Allen, … Rajesh Khanna·PainPeer-reviewed·Sep 26, 2023
- A chemogenetic ligand-receptor pair for voltage-gated sodium channel subtype-selective inhibition
Elizabeth R. Park, Nicholas Denomme, … J. Du Bois·bioRxiv·Nov 3, 2025
- Discovery of a Selective, State-Independent Inhibitor of NaV1.7 by Modification of Guanidinium Toxins
Hassan Pajouhesh, Jacob T. Beckley, … John V. Mulcahy·Scientific ReportsPeer-reviewed·Sep 9, 2020
- Nav1.7 gating in human iPSC derived sensory neurons: an experimental and computational study
Alberto Capurro, Jack R. Thornton, … Evelyne Sernagor·bioRxiv·Aug 4, 2020