ArticlePloS one2014
Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Voltage-gated sodium channel 1.8 contributes to hyperalgesia induced by the coexistence of anxiety and remifentanil exposure.The Korean journal of pain · 2026Article
- Toward Brain NaPharmaceuticals (Basel, Switzerland) · 2025Article
- Contusive spinal cord injury causes Nav1.8 dysfunction to upregulate small sensory neuron excitability.The Journal of physiology · 2025Article
- Lidocaine-A Promising Candidate for the Treatment of Cancer-Induced Bone Pain: A Narrative Review.Advances in therapy · 2025Review
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- Protein Misfolding and Aggregation as a Mechanistic Link Between Chronic Pain and Neurodegenerative Diseases.Current issues in molecular biology · 2025Review
- Peripheral Mechanism of Cancer-Induced Bone Pain.Neuroscience bulletin · 2024Review
- Chemogenetic Silencing of NaeNeuro · 2023Article
- Novel Therapies for the Treatment of Neuropathic Pain: Potential and Pitfalls.Journal of clinical medicine · 2022Review
- Prostaglandin ERespiratory research · 2021Article
- Genetic Variations and Health-Related Quality of Life (HRQOL): A Genome-Wide Study Approach.Cancers · 2021Article
- The Potential Effect of NaFrontiers in molecular neuroscience · 2021Article
- Intercellular communication and ion channels in neuropathic pain chronicization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Adaptive mechanisms driving maladaptive pain: how chronic ongoing activity in primary nociceptors can enhance evolutionary fitness after severe injury.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- The NaFrontiers in pharmacology · 2018Review
- Sodium Channel NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Modulation of Nav1.8 by Lysophosphatidic Acid in the Induction of Bone Cancer Pain.Neuroscience bulletin · 2016Article
- Hyperexcitability and sensitization of sodium channels of dorsal root ganglion neurons in a rat model of lumber disc herniation.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2016Article
- Upregulation of bone morphogenetic protein 2 ( Bmp2) in dorsal root ganglion in a rat model of bone cancer pain.Molecular painArticle
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. We speculate that the Nav1.8 sodium channel is a potential candidate responsible for the enhanced excitability of DRG neurons in rats with bone cancer pain. Here, using electrophysiology, Western blot and behavior assays, we documented that the current density of TTX-R sodium channels, especially the Nav1.8 channel, increased significantly in DRG neurons of rats with cancer-induced bone pain. This increase may be due to an increased expression of Nav1.8 on the membrane of DRG neurons. Accordantly, blockade of Nav1.8 sodium channels by its selective blocker A-803467 significantly alleviated the cancer-induced mechanical allodynia and thermal hyperalgesia in rats. Taken together, these results suggest that functional upregulation of Nav1.8 channels on the membrane of DRG neurons contributes to the development of cancer-induced bone pain.
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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.