ArticleMolecular and cellular neurosciences2009
Loss of Na+ channel beta2 subunits is neuroprotective in a mouse model of multiple sclerosis.
Article in Molecular and cellular neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- miR-449a modulates Alzheimer's disease pathology through regulation of Navβ2.Zoological research · 2026Article
- Navβ2 Intracellular Fragments Contribute to Aβ1-42-Induced Cognitive Impairment and Synaptic Deficit Through Transcriptional Suppression of BDNF.Molecular neurobiology · 2025Article
- Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by ANeural plasticity · 2022Article
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- MicroRNA‑449a regulates the progression of brain aging by targeting SCN2B in SAMP8 mice.International journal of molecular medicine · 2020Article
- Nav1.6 promotes inflammation and neuronal degeneration in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2019Article
- Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease.Neuropharmacology · 2018Review
- Voltage-Gated Sodium Channel β Subunits and Their Related Diseases.Handbook of experimental pharmacology · 2018Review
- Navβ2 knockdown improves cognition in APP/PS1 mice by partially inhibiting seizures and APP amyloid processing.Oncotarget · 2017Article
- Distribution and function of voltage-gated sodium channels in the nervous system.Channels (Austin, Tex.) · 2017Review
- Sodium Channel β2 Subunits Prevent Action Potential Propagation Failures at Axonal Branch Points.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The influence of sodium on pathophysiology of multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
- SCN2B in the Rat Trigeminal Ganglion and Trigeminal Sensory Nuclei.Cellular and molecular neurobiology · 2016Article
- Sodium Channel Voltage-Gated Beta 2 Plays a Vital Role in Brain Aging Associated with Synaptic Plasticity and Expression of COX5A and FGF-2.Molecular neurobiology · 2016Article
- Article
- Sodium MRI of multiple sclerosis.NMR in biomedicine · 2016Review
- Sodium channel β subunits: emerging targets in channelopathies.Annual review of physiology · 2015Review
- Dual roles of voltage-gated sodium channels in development and cancer.The International journal of developmental biology · 2015Review
- Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis.Nature reviews. Neurology · 2014Review
- Sodium channel β2 subunit promotes filopodia-like processes and expansion of the dendritic tree in developing rat hippocampal neurons.Frontiers in cellular neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a CNS disease that includes demyelination and axonal degeneration. Voltage-gated Na+ channels are abnormally expressed and distributed in MS and its animal model, Experimental Allergic Encephalomyelitis (EAE). Up-regulation of Na+ channels along demyelinated axons is proposed to lead to axonal loss in MS/EAE. We hypothesized that Na+ channel beta2 subunits (encoded by Scn2b) are involved in MS/EAE pathogenesis, as beta2 is responsible for regulating levels of channel cell surface expression in neurons. We induced non-relapsing EAE in Scn2b(+/+) and Scn2b(-/-) mice on the C57BL/6 background. Scn2b(-/-) mice display a dramatic reduction in EAE symptom severity and lethality as compared to wildtype, with significant decreases in axonal degeneration and axonal loss. Scn2b(-/-) mice show normal peripheral immune cell populations, T cell proliferation, cytokine release, and immune cell infiltration into the CNS in response to EAE, suggesting that Scn2b inactivation does not compromise immune function. Our data suggest that loss of beta2 is neuroprotective in EAE by prevention of Na+ channel up-regulation in response to demyelination.
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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.