Article

Biophysical Characterization of the human Nav1.9 sodium channel in trigeminal ganglia and dorsal root ganglia neurons

2026-08-25

Abstract excerpt

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 is...

Topics

Open a Topic to create a Post that cites this publication.

Uncategorized literature

Identifiers and source

Literature Corpus work: 0f8075fa-59d5-500a-9aa3-9d7b7d619d24
DOI: 10.64898/2026.08.22.746445

Open publication

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Click a neighbor to travelStep 1 · 12 closest

Biophysical Characterization of the human Nav1.9 sodium channel in trigeminal ganglia and dorsal root ganglia neuronsDOI 10.64898/2026.08.22.746445Read

Understanding the physiological role of NaV1.9: Challenges and opportunities for pain modulation.Semantic proximity Read

Sodium channelopathies and pain.Semantic proximity Read

Preclinical Animal Models to Investigate the Role of Nav1.7 Ion Channels in PainSemantic proximity Read

Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitabilitySemantic proximity Read

Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain.Semantic proximity Read

Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels.Semantic proximity Read

The Role of Voltage-Gated Sodium Channels in Pain SignalingSemantic proximity Read

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.Semantic proximity Read

NaV1.9: a sodium channel linked to human pain.Semantic proximity Read

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

NaV1.8/NaV1.9 double deletion mildly affects acute pain responses in miceSemantic proximity Read

Painful and painless channelopathies.Semantic proximity Read