ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Increased Resurgent Sodium Currents in Nav1.8 Contribute to Nociceptive Sensory Neuron Hyperexcitability Associated with Peripheral Neuropathies.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.The Journal of physiology · 2026Article
- Review
- Sodium Channel Inhibitors in Clinical Development for Pain Management: A Focused Review.CNS drugs · 2026Review
- Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- From ion channel biology to clinical practice: suzetrigine as a precision analgesic.Frontiers in medicine · 2026Review
- A novel platelet-rich plasma clinically induces reliable, rapid, long-term chronic peripheral neuropathic pain elimination.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- Contusive spinal cord injury causes Nav1.8 dysfunction to upregulate small sensory neuron excitability.The Journal of physiology · 2025Article
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- Voltage-Gated Sodium Channel Dysfunction in Epilepsy: Zebrafish Models for Therapeutics.Biomedicines · 2025Review
- Review
- Review
- Modulation of human dorsal root ganglion neuron firing by the Nav1.8 inhibitor suzetrigine.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- Human sensory neurons exhibit cell-type-specific, pain-associated differences in intrinsic excitability and expression ofbioRxiv : the preprint server for biology · 2025Article
- Article
- Molecular determinants of resurgent sodium currents mediated by Navβ4 peptide and A-type FHFs.Frontiers in molecular neuroscience · 2024Article
- Unveiling adcyap1 as a protective factor linking pain and nerve regeneration through single-cell RNA sequencing of rat dorsal root ganglion neurons.BMC biology · 2023Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- Exploring gene signatures and regulatory networks in a rat model of sciatica: implications and validation in neuropathic pain.Frontiers in molecular neuroscience · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Neuropathic pain is a significant public health challenge, yet the underlying mechanisms remain poorly understood. Painful small fiber neuropathy (SFN) may be caused by gain-of-function mutations in Nav1.8, a sodium channel subtype predominantly expressed in peripheral nociceptive neurons. However, it is not clear how Nav1.8 disease mutations induce sensory neuron hyperexcitability. Here we studied two mutations in Nav1.8 associated with hypersensitive sensory neurons: G1662S reported in painful SFN; and T790A, which underlies increased pain behaviors in the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.