ArticleThe Journal of clinical investigation2023
Neuron-oligodendrocyte potassium shuttling at nodes of Ranvier protects against inflammatory demyelination.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Activity-dependent COeLife · 2026Article
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Channel Dysfunction as the Basis for Comorbidities in Multiple Sclerosis and Depression.Archiv der Pharmazie · 2026Review
- From Retigabine to Azetukalner: Reviving Voltage-Gated Potassium Channels for Epilepsy Therapy.Archiv der Pharmazie · 2026Review
- Mapping the secondary response to traumatic brain injury using spatial transcriptomics shows acute 4-aminopyridine treatment mitigates axonal and molecular pathology.Acta neuropathologica communications · 2026Article
- TREK1 Channels Shape Spindle-Like Oscillations, Neuronal Activity, and Short-Term Synaptic Plasticity in Thalamocortical Circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Spironolactone Targets Retinoid X Receptor γ to Promote Myelin Sheath Regeneration.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
- Single-Cell RNA Sequencing and Spatial Transcriptomics Reveal a Novel Mechanism of Oligodendrocyte-Neuron Interaction in Cognitive Decline After High-Altitude Cerebral Edema.CNS neuroscience & therapeutics · 2025Article
- Neuroinflammation causes mitral cell dysfunction and olfactory impairment in a multiple sclerosis model.Journal of neuroinflammation · 2025Article
- Transcriptomic profiling identifies ferroptosis and NF-κB signaling involved in α-dimorphecolic acid regulation of microglial inflammation.Journal of translational medicine · 2025Article
- Review
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Article
- Wrap it up: myelination of transplanted neurons for repair.Frontiers in cellular neuroscience · 2025Review
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- ICA-27243 improves neuromuscular function and preserves motoneurons in the transgenic SOD1Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Mechanisms of axonal support by oligodendrocyte-derived extracellular vesicles.Nature reviews. Neuroscience · 2023Review
- Seeking neuroprotection in multiple sclerosis: an ongoing challenge.The Journal of clinical investigation · 2023Article
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42 authors at 19 institutions in 8 countries.
Funding
Abstract
Multiple sclerosis (MS) is a progressive inflammatory demyelinating disease of the CNS. Increasing evidence suggests that vulnerable neurons in MS exhibit fatal metabolic exhaustion over time, a phenomenon hypothesized to be caused by chronic hyperexcitability. Axonal Kv7 (outward-rectifying) and oligodendroglial Kir4.1 (inward-rectifying) potassium channels have important roles in regulating neuronal excitability at and around the nodes of Ranvier. Here, we studied the spatial and functional relationship between neuronal Kv7 and oligodendroglial Kir4.1 channels and assessed the transcriptional and functional signatures of cortical and retinal projection neurons under physiological and inflammatory demyelinating conditions. We found that both channels became dysregulated in MS and experimental autoimmune encephalomyelitis (EAE), with Kir4.1 channels being chronically downregulated and Kv7 channel subunits being transiently upregulated during inflammatory demyelination. Further, we observed that pharmacological Kv7 channel opening with retigabine reduced neuronal hyperexcitability in human and EAE neurons, improved clinical EAE signs, and rescued neuronal pathology in oligodendrocyte-Kir4.1-deficient (OL-Kir4.1-deficient) mice. In summary, our findings indicate that neuron-OL compensatory interactions promoted resilience through Kv7 and Kir4.1 channels and identify pharmacological activation of nodal Kv7 channels as a neuroprotective strategy against inflammatory demyelination.
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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.