ArticleNeurochemical research2003
Initiation of sodium channel clustering at the node of Ranvier in the mouse optic nerve.
Article in Neurochemical research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Paranodal Axoglial Junctions, an Essential Component in Axonal Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Microglial process convergence on axonal segments in health and disease.Neuroimmunology and neuroinflammation · 2020Article
- Human intraretinal myelination: axon diameters and axon/myelin thickness ratios.Indian journal of ophthalmology · 2013Article
- Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Age-related molecular reorganization at the node of Ranvier.The Journal of comparative neurology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion fluxes in mammalian myelinated axons are restricted to the nodes of Ranvier, where, in particular, voltage-gated Na+ channels are clustered at a high density. The node of Ranvier is separated from the internode by two distinct domains of the axolemma, the paranode and the juxtaparanode. Each axonal domain is characterized by the presence of a specific protein complex. Although oligodendrocytes and/or myelin membranes are believed to play some instructive roles in the organization of axonal domains, the mechanisms leading to their localized distribution are not well understood. In this paper we focused on the involvement of myelin sheaths in this domain organization and examined the distribution of axonal components in the optic nerves of wild type, hypomyelinatingjimpy mice and demyelinating PLP transgenic mice. The results showed that the clustering of Na+ channels does not require junction-like structures to be formed between the glial processes and axons, but requires mature oligodendrocytes to be present in close vicinity.
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Registered trials
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