ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Sodium channel Na(v)1.7 is essential for lowering heat pain threshold after burn injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 102 citations in OpenAlex.
- Burn Selection: How Fire Injury Shaped Human Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- Molecular Mechanisms Underlying Burn-Injury Induced Pain: From Inflammation to Epigenetics.Military medicine · 2025Review
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Discovery and development of an oral analgesic targeting the α2B adrenoceptor.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
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Advancing Pain Understanding and Drug Discovery: Insights from Preclinical Models and Recent Research Findings.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Non-severe thermal burn injuries induce long-lasting downregulation of gene expression in cortical excitatory neurons and microglia.Frontiers in molecular neuroscience · 2024Article
- Gene therapy for chronic pain: emerging opportunities in target-rich peripheral nociceptors.Nature reviews. Neuroscience · 2023Review
- Conserved but not critical: Trafficking and function of NaFrontiers in molecular neuroscience · 2023Article
- Computational design of peptides to target NaeLife · 2022Article
- Multifactorial pathways in burn injury-induced chronic pain: novel targets and their pharmacological modulation.Molecular biology reports · 2022Review
- Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons.Journal of neurophysiology · 2022Article
- Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway.International journal of molecular sciences · 2022Review
- Normalization of Neuroinflammation: A New Strategy for Treatment of Persistent Pain and Memory/Emotional Deficits in Chronic Pain.Journal of inflammation research · 2022Review
- The impact of foot shock-induced stress on pain-related behavior associated with burn injury.Burns : journal of the International Society for Burn Injuries · 2021Article
- Nociceptor Overexpression of NaThe journal of pain · 2021Article
- Long-lasting analgesia via targeted in situ repression of NaScience translational medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marked hypersensitivity to heat and mechanical (pressure) stimuli develop after a burn injury, but the neural mechanisms underlying these effects are poorly understood. In this study, we establish a new mouse model of focal second-degree burn injury to investigate the molecular and cellular basis for burn injury-induced pain. This model features robust injury-induced behavioral effects and tissue-specific altered cytokine profile, but absence of glial activation in spinal dorsal horn. Three voltage-gated sodium channels, Na(v)1.7, Na(v)1.8, and Na(v)1.9, are preferentially expressed in peripheral somatosensory neurons of the dorsal root ganglia (DRGs) and have been implicated in injury-induced neuronal hyperexcitability. Using knock-out mice, we provide evidence that Na(v)1.7 selectively contributes to burn-induced hypersensitivity to heat, but not mechanical, stimuli. After burn model injury, wild-type mice display increased sensitivity to heat stimuli, and a normally non-noxious warm stimulus induces activity-dependent Fos expression in spinal dorsal horn neurons. Strikingly, both effects are absent in Na(v)1.7 conditional knock-out (cKO) mice. Furthermore, burn injury increases density and shifts activation of tetrodotoxin-sensitive currents in a hyperpolarized direction, both pro-excitatory properties, in DRG neurons from wild-type but not Na(v)1.7 cKO mice. We propose that, in sensory neurons damaged by burn injury to the hindpaw, Na(v)1.7 currents contribute to the hyperexcitability of sensory neurons, their communication with postsynaptic spinal pain pathways, and behavioral thresholds to heat stimuli. Our results offer insights into the molecular and cellular mechanisms of modality-specific pain signaling, and suggest Na(v)1.7-blocking drugs may be effective in burn patients.
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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.