NaV1.7 nociceptor sodium channel
Selected indexed studies
- Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids. (Neuron, 2023) [PMID:37352856]
- Human pain channelopathies. (Handb Clin Neurol, 2024) [PMID:39174256]
- Network topology of NaV1.7 mutations in sodium channel-related painful disorders. (BMC Syst Biol, 2017) [PMID:28235406]
_Worker-drafted node — pending editorial review._
Connections
No connections recorded yet.
Sources
- Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids. (2023) pubmed
- Human pain channelopathies. (2024) pubmed
- Network topology of NaV1.7 mutations in sodium channel-related painful disorders. (2017) pubmed
- Modulation of human dorsal root ganglion neuron firing by the Nav1.8 inhibitor suzetrigine. (2025) pubmed
- Pharmacologic Characterization of LTGO-33, a Selective Small Molecule Inhibitor of the Voltage-Gated Sodium Channel Na(V)1.8 with a Unique Mechanism of Action. (2024) pubmed
- The analgesic paracetamol metabolite AM404 acts peripherally to directly inhibit sodium channels. (2025) pubmed
- A nociceptor excitability test for identifying alterations of the Nav1.7 channels in humans. (2026) pubmed
- An approach to targeting Nav1.7 for pain sensations. (2025) pubmed
- Nav1.8, an analgesic target for nonpsychotomimetic phytocannabinoids. (2025) pubmed
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials. (2025) pubmed