ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Leukoencephalopathy upon disruption of the chloride channel ClC-2.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
What it found
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Who cites it
106 citing papers in PubMed, 173 citations in OpenAlex.
- Orchestrating brain fluid dynamics: circadian regulation of CSF, glymphatic exchange, and waste clearance.Frontiers in cell and developmental biology · 2026Review
- Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy.Molecular psychiatry · 2026Article
- Identification of a novelFrontiers in genetics · 2026Article
- Glial Ion Channels in Myelin Pathophysiology: Insights from Leukodystrophies.Life (Basel, Switzerland) · 2025Review
- The loss of a ClC anion channel increases life span, health span, and stress resistance by alkalinizing a pair of glial cells inScience advances · 2025Article
- Regulation of testosterone synthesis in Leydig cells by ClC-2 chloride channel.Reproduction (Cambridge, England) · 2025Article
- A Theoretical and Practical Analysis of Membrane Protein Genes Altered in Neutrophils in Parkinson's Disease.Current issues in molecular biology · 2025Article
- Regulatory and disruptive variants in the CLCN2 gene are associated with modified skin color pattern phenotypes in the corn snake.Genome biology · 2025Article
- Review
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Role of voltage-gated chloride channels in epilepsy: current insights and future directions.Frontiers in pharmacology · 2025Review
- Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2024Review
- Article
- Expanding the phenotypic spectrum ofBrain communications · 2024Article
- A helping hand: roles for accessory cells in the sense of touch across species.Frontiers in cellular neuroscience · 2024Review
- Adrenal Anion Channels: New Roles in Zona Glomerulosa Physiology and in the Pathophysiology of Primary Aldosteronism.Handbook of experimental pharmacology · 2024Article
- Morphological and Molecular Changes in the Cortex and Cerebellum of Immunocompetent Mice Infected with Zika Virus.Viruses · 2023Article
- Article
- Cryo-EM structures of ClC-2 chloride channel reveal the blocking mechanism of its specific inhibitor AK-42.Nature communications · 2023Article
- Biallelic CLCN2 mutations cause retinal degeneration by impairing retinal pigment epithelium phagocytosis and chloride channel function.Human genetics · 2023Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ClC-2 is a broadly expressed plasma membrane chloride channel that is modulated by voltage, cell swelling, and pH. A human mutation leading to a heterozygous loss of ClC-2 has previously been reported to be associated with epilepsy, whereas the disruption of Clcn2 in mice led to testicular and retinal degeneration. We now show that the white matter of the brain and spinal cord of ClC-2 knock-out mice developed widespread vacuolation that progressed with age. Fluid-filled spaces appeared between myelin sheaths of the central but not the peripheral nervous system. Neuronal morphology, in contrast, seemed normal. Except for the previously reported blindness, neurological deficits were mild and included a decreased conduction velocity in neurons of the central auditory pathway. The heterozygous loss of ClC-2 had no detectable functional or morphological consequences. Neither heterozygous nor homozygous ClC-2 knock-out mice had lowered seizure thresholds. Sequencing of a large collection of human DNA and electrophysiological analysis showed that several ClC-2 sequence abnormalities previously found in patients with epilepsy most likely represent innocuous polymorphisms.
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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.