ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Altered ion channels in an animal model of Charcot-Marie-Tooth disease type IA.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 78 citations in OpenAlex.
- Chemogenetic Schwann cell activation impairs early myelination and triggers adult demyelination in the peripheral nervous system.Frontiers in cellular neuroscience · 2026Article
- Distinct Changes in Calpain and Calpastatin during PNS Myelination and Demyelination in Rodent Models.International journal of molecular sciences · 2022Article
- Two distinct types of nodes of Ranvier support auditory nerve function in the mouse cochlea.Glia · 2022Article
- New evidence for secondary axonal degeneration in demyelinating neuropathies.Neuroscience letters · 2021Review
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- Neuropeptides and the Nodes of Ranvier in Cranial Headaches.Frontiers in physiology · 2021Review
- Familial trigeminal neuralgia - a systematic clinical study with a genomic screen of the neuronal electrogenisome.Cephalalgia : an international journal of headache · 2020Article
- Axonal Spectrins: Nanoscale Organization, Functional Domains and Spectrinopathies.Frontiers in cellular neuroscience · 2019Review
- Caveats in the Established Understanding of CMT1A.Annals of clinical and translational neurology · 2017Article
- Article
- Mechanisms of sodium channel clustering and its influence on axonal impulse conduction.Cellular and molecular life sciences : CMLS · 2016Review
- Charcot-Marie-Tooth disease: New insights from skin biopsy.Neurology · 2015Article
- Molecular regulators of nerve conduction - Lessons from inherited neuropathies and rodent genetic models.Experimental neurology · 2015Review
- Myelin damage and repair in pathologic CNS: challenges and prospects.Frontiers in molecular neuroscience · 2015Review
- Neuro-glial interactions at the nodes of Ranvier: implication in health and diseases.Frontiers in cellular neuroscience · 2013Review
- Node of Ranvier disruption as a cause of neurological diseases.ASN neuro · 2013Review
- The PMP22 gene and its related diseases.Molecular neurobiology · 2013Review
- An essential role of MAG in mediating axon-myelin attachment in Charcot-Marie-Tooth 1A disease.Neurobiology of disease · 2013Article
- Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions.Frontiers in cellular neuroscience · 2013Article
- Modulation of voltage-gated K+ channels by the sodium channel β1 subunit.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
How demyelination and remyelination affect the function of myelinated axons is a fundamental aspect of demyelinating diseases. We examined this issue in Trembler-J mice, a genetically authentic model of a dominantly inherited demyelinating neuropathy of humans. The K+ channels Kv1.1 and Kv1.2 channels were often improperly located in the paranodal axon membrane, typically associated with improperly formed paranodes, and in unmyelinated segments between internodes. As in wild-type nerves, Trembler-J nodes contained Nav1.6, ankyrin-G, betaIV-spectrin, and KCNQ2, but, unlike wild-type nerves, they also contained Kv3.1b and Nav1.8. In unmyelinated segments bordered by myelin sheaths, these proteins were clustered in heminodes and did not appear to be diffusely localized in the unmyelinated segments themselves. Nodes and heminodes were contacted by Schwann cells processes that did not have the ultrastructural or molecular characteristics of mature microvilli. Despite the presence of Nav1.8, a tetrodotoxin-resistant sodium channel, sciatic nerve conduction was at least as sensitive to tetrodotoxin in Trembler-J nerves as in wild-type nerves. Thus, the profound reorganization of axonal ion channels and the aberrant expression of novel ion channels likely contribute to the altered conduction in Trembler-J nerves.
Indexed as
Identifiers
What OpenQuestion holds
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.