ArticleeLife2016
Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Degraded myelin is associated with cold hypersensitivity in paclitaxel-induced peripheral neuropathy.bioRxiv : the preprint server for biology · 2026Article
- Pharmacological Actions of Potassium Channel Openers on Voltage-Gated Potassium Channels.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Role of voltage-gated CaJournal of neurophysiology · 2025Article
- Specific overexpression of contactin-associated protein-like 2 and its effects on pain-related behaviour in mice.Pain reports · 2025Article
- KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A role for leucine-rich, glioma inactivated 1 in regulating pain sensitivity.Brain : a journal of neurology · 2025Article
- From arthritis to central sensitization: targeting the neuro-immune axis via microglial modulation in acupuncture treatment for Juvenile Idiopathic Arthritis-associated pain.Frontiers in immunology · 2025Review
- A functional unbalance of TRPM8 and Kv1 channels underlies orofacial cold allodynia induced by peripheral nerve damage.Frontiers in pharmacology · 2024Article
- The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Review
- The structure of sensory afferent compartments in health and disease.Journal of anatomy · 2022Review
- Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury.Acta neuropathologica communications · 2022Article
- miR-155-5p in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain.Molecular pain · 2022Article
- A population ofF1000Research · 2022Article
- [Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management : German version].Schmerz (Berlin, Germany) · 2021Review
- Studying IndependentThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Silent cold-sensing neurons contribute to cold allodynia in neuropathic pain.Brain : a journal of neurology · 2021Article
- Human Oligodendrocytes and Myelin In Vitro to Evaluate Developmental Neurotoxicity.International journal of molecular sciences · 2021Review
- Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain.International journal of molecular sciences · 2021Review
- Functional Differences Between Two Kv1.1 RNA Editing Isoforms: a Comparative Study on Neuronal Overexpression in Mouse Prefrontal Cortex.Molecular neurobiology · 2021Article
- Functional Coupling of Slack Channels and P2X3 Receptors Contributes to Neuropathic Pain Processing.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury.
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Registered trials
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