ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Sensory neuron downregulation of the Kv9.1 potassium channel subunit mediates neuropathic pain following nerve 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. It is linked to trial NCT05712980 (Identification of Differentially Expressed Genes in RNAseq Data of Patients With Failed Back Surgery Syndrome Treated With Different Modalities of Spinal Cord Stimulation), which is not on this map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Identification of Differentially Expressed Genes in RNAseq Data of Patients With Failed Back Surgery Syndrome Treated With Different Modalities of Spinal Cord Stimulation: Looking for Biomarkers of Response and Effectiveness
Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Systematic Review and Meta-Analysis of Genetic Risk of Developing Chronic Postsurgical Pain.The journal of painPooled it
- Article
- Mechanistic correlation of potassium channel sensing and nitric oxide activity in neuroinflammation.Molecular biology reports · 2025Review
- Review
- A Kv2 inhibitor combination reveals native neuronal conductances consistent with Kv2/KvS heteromers.eLife · 2025Article
- Regulation of Kv2.1 Channels by Kv9.1 Variants.Biomedicines · 2025Article
- Ion Channel and Transporter Involvement in Chemotherapy-Induced Peripheral Neurotoxicity.International journal of molecular sciences · 2024Review
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KThe Journal of comparative neurology · 2024Article
- Gut Microbiota Modulation and Its Implications on Neuropathic Pain: A Comprehensive Literature Review.Pain and therapy · 2024Review
- A novel approach to completely alleviate peripheral neuropathic pain in human patients: insights from preclinical data.Frontiers in neuroanatomy · 2024Review
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KbioRxiv : the preprint server for biology · 2023Article
- Ion Channel Genes in Painful Neuropathies.Biomedicines · 2023Review
- Gene therapy for chronic pain: emerging opportunities in target-rich peripheral nociceptors.Nature reviews. Neuroscience · 2023Review
- Unveiling the mechanisms of neuropathic pain suppression: perineural resiniferatoxin targets Trpv1 and beyond.Frontiers in neuroanatomy · 2023Article
- Ion channel long non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2022Review
- Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021Review
- Kcns3 deficiency disrupts Parvalbumin neuron physiology in mouse prefrontal cortex: Implications for the pathophysiology of schizophrenia.Neurobiology of disease · 2021Article
- Functional Coupling of Slack Channels and P2X3 Receptors Contributes to Neuropathic Pain Processing.International journal of molecular sciences · 2021Article
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Antispasmodic Drug Drofenine as an Inhibitor of Kv2.1 Channel Ameliorates Peripheral Neuropathy in Diabetic Mice.iScience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic neuropathic pain affects millions of individuals worldwide, is typically long-lasting, and remains poorly treated with existing therapies. Neuropathic pain arising from peripheral nerve lesions is known to be dependent on the emergence of spontaneous and evoked hyperexcitability in damaged nerves. Here, we report that the potassium channel subunit Kv9.1 is expressed in myelinated sensory neurons, but is absent from small unmyelinated neurons. Kv9.1 expression was strongly and rapidly downregulated following axotomy, with a time course that matches the development of spontaneous activity and pain hypersensitivity in animal models. Interestingly, siRNA-mediated knock-down of Kv9.1 in naive rats led to neuropathic pain behaviors. Diminished Kv9.1 function also augmented myelinated sensory neuron excitability, manifested as spontaneous firing, hyper-responsiveness to stimulation, and persistent after-discharge. Intracellular recordings from ex vivo dorsal root ganglion preparations revealed that Kv9.1 knock-down was linked to lowered firing thresholds and increased firing rates under physiologically relevant conditions of extracellular potassium accumulation during prolonged activity. Similar neurophysiological changes were detected in animals subjected to traumatic nerve injury and provide an explanation for neuropathic pain symptoms, including poorly understood conditions such as hyperpathia and paresthesias. In summary, our results demonstrate that Kv9.1 dysfunction leads to spontaneous and evoked neuronal hyperexcitability in myelinated fibers, coupled with development of neuropathic pain behaviors.
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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.