ArticleBMC neuroscience2017
Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma.
Article in BMC neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders.Translational psychiatry · 2018Pooled it
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- A comprehensive mechanism of biological and health effects of anthropogenic extremely low frequency and wireless communication electromagnetic fields.Frontiers in public health · 2025Review
- Electrical stimulation for the treatment of spinal cord injuries: A review of the cellular and molecular mechanisms that drive functional improvements.Frontiers in cellular neuroscience · 2023Review
- Human‑made electromagnetic fields: Ion forced‑oscillation and voltage‑gated ion channel dysfunction, oxidative stress and DNA damage (Review).International journal of oncology · 2021Review
- Use of Gene Therapy in Retinal Ganglion Cell Neuroprotection: Current Concepts and Future Directions.Biomolecules · 2021Review
- Neuron to Oligodendrocyte Precursor Cell Synapses: Protagonists in Oligodendrocyte Development and Myelination, and Targets for Therapeutics.Frontiers in neuroscience · 2021Review
- Editorial: Ion Channels: Therapeutic Targets for Neurological Disease.Frontiers in molecular neuroscience · 2021Article
- Article
- Protein corona formation moderates the release kinetics of ion channel antagonists from transferrin-functionalized polymeric nanoparticles.RSC advances · 2020Article
- The correlation and role analysis of KCNK2/4/5/15 in Human Papillary Thyroid Carcinoma microenvironment.Journal of Cancer · 2020Article
- Acute Cellular and Functional Changes With a Combinatorial Treatment of Ion Channel Inhibitors Following Spinal Cord Injury.Frontiers in molecular neuroscience · 2020Article
- A Network Pharmacology Approach to Explore the Potential Mechanisms of Yifei Sanjie Formula in Treating Pulmonary Fibrosis.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- CaCellular and molecular neurobiology · 2019Review
- Comparing modes of delivery of a combination of ion channel inhibitors for limiting secondary degeneration following partial optic nerve transection.Scientific reports · 2019Article
- Quantitative profiling of regional protein expression in rat retina after partial optic nerve transection using fluorescence difference two‑dimensional gel electrophoresis.Molecular medicine reports · 2019Article
- Rapid Repeat Exposure to Subthreshold Trauma Causes Synergistic Axonal Damage and Functional Deficits in the Visual Pathway in a Mouse Model.Journal of neurotrauma · 2019Article
- Voluntary running delays primary degeneration in rat retinas after partial optic nerve transection.Neural regeneration research · 2019Article
- Comparison of ion channel inhibitor combinations for limiting secondary degeneration following partial optic nerve transection.Experimental brain research · 2019Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFollowing partial injury to the central nervous system, cells beyond the initial injury site undergo secondary degeneration, exacerbating loss of neurons, compact myelin and function. Changes in Ca
resultsFollowing partial optic nerve transection, hyper-phosphorylation of Tau and acetylated tubulin immunoreactivity were increased, and Nogo-A immunoreactivity was decreased, indicating that axonal changes occurred acutely. All combinations of ion channel inhibitors reduced hyper-phosphorylation of Tau and increased Nogo-A immunoreactivity at day 3 after injury. However, only Lom/oxATP or all three inhibitors in combination significantly reduced acetylated tubulin immunoreactivity. Most combinations of ion channel inhibitors were effective in restoring the lengths of the paranode and the paranodal gap, indicative of the length of the node of Ranvier, following injury. However, only all three inhibitors in combination restored to normal Ankyrin G length at the node of Ranvier. Similarly, HNE immunoreactivity and loss of oligodendrocyte precursor cells were only limited by treatment with all three ion channel inhibitors in combination.
conclusionsData indicate that inhibiting any of a range of ion channels preserves certain elements of axon and node structure and limits some oxidative damage following injury, whereas ionic flux through all three channels must be inhibited to prevent lipid peroxidation and preserve Ankyrin G distribution and OPCs.
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