ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Kir4.1 potassium channel subunit is crucial for oligodendrocyte development and in vivo myelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.
What it found
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Who cites it
152 citing papers in PubMed, 295 citations in OpenAlex.
- Beyond Neurodegeneration: White Matter Vacuolation as a Primary Myelin Defect.International journal of molecular sciences · 2026Review
- Gender-Associated Differences in the Regulation of Potassium Channels in Astrocytes of Type 2 Diabetic Mice.Cells · 2026Article
- Müller cell markers in aqueous humor of patients with type-2 macular telangiectasia.Indian journal of ophthalmology · 2026Article
- Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy.Molecular psychiatry · 2026Article
- A pH-responsive and self-healing CEC/PEG-(CHO)Frontiers in neuroscience · 2026Article
- Glial Ion Channels in Myelin Pathophysiology: Insights from Leukodystrophies.Life (Basel, Switzerland) · 2025Review
- Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Roles of Ion Channels in Oligodendrocyte Precursor Cells: From Physiology to Pathology.International journal of molecular sciences · 2025Review
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Axonal neurotransmitter release in the regulation of myelination.Bioscience reports · 2024Review
- Pharmacological inhibition of Kir4.1 evokes rapid-onset antidepressant responses.Nature chemical biology · 2024Article
- Oligodendrocyte-axon metabolic coupling is mediated by extracellular KNature neuroscience · 2024Article
- Spontaneous mutation in 2310061I04Rik results in reduced expression of mitochondrial genes and impaired brain myelination.PloS one · 2024Article
- Altered calcium signaling in Bergmann glia contributes to spinocerebellar ataxia type-1 in a mouse model of SCA1.Neurobiology of disease · 2023Article
- Transplantation of neural stem progenitor cells from different sources for severe spinal cord injury repair in rat.Bioactive materials · 2023Article
- Mechanisms of Diseases Associated with Mutation in GJC2/Connexin 47.Biomolecules · 2023Review
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- CNS myelination requires VAMP2/3-mediated membrane expansion in oligodendrocytes.Nature communications · 2022Article
- Kir5.1 channels: potential role in epilepsy and seizure disorders.American journal of physiology. Cell physiology · 2022Review
92 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
To understand the cellular and in vivo functions of specific K(+) channels in glia, we have studied mice with a null mutation in the weakly inwardly rectifying K(+) channel subunit Kir4.1. Kir4.1-/- mice display marked motor impairment, and the cellular basis is hypomyelination in the spinal cord, accompanied by severe spongiform vacuolation, axonal swellings, and degeneration. Immunostaining in the spinal cord of wild-type mice up to postnatal day 18 reveals that Kir4.1 is expressed in myelin-synthesizing oligodendrocytes, but probably not in neurons or glial fibrillary acidic protein-positive (GFAP-positive) astrocytes. Cultured oligodendrocytes from developing spinal cord of Kir4.1-/- mice lack most of the wild-type K(+) conductance, have depolarized membrane potentials, and display immature morphology. By contrast, cultured neurons from spinal cord of Kir4.1-/- mice have normal physiological characteristics. We conclude that Kir4.1 forms the major K(+) conductance of oligodendrocytes and is therefore crucial for myelination. The Kir4.1 knock-out mouse is one of the few CNS dysmyelinating or demyelinating phenotypes that does not involve a gene directly involved in the structure, synthesis, degradation, or immune response to myelin. Therefore, this mouse shows how an ion channel mutation could contribute to the polygenic demyelinating diseases.
Indexed as
Identifiers
11466414PMC6762664W2164584173What 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.