ArticleBrain communications2020
Increased glutamate transporter-associated anion currents cause glial apoptosis in episodic ataxia 6.
Article in Brain communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 35 citations in OpenAlex.
- Overactive EAAT1 ClActa neuropathologica communications · 2026Article
- Multimodal dynamics control activity of a glial glutamate transporter.bioRxiv : the preprint server for biology · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- The severity of SLC1A2-associated neurodevelopmental disorders correlates with transporter dysfunction.EBioMedicine · 2025Article
- Astrocyte chloride, excitatory-inhibitory balance and epilepsy.Neural regeneration research · 2024Article
- Both Enantiomers of 2-Hydroxyglutarate Modulate the Metabolism of Cultured Human Neuroblastoma Cells.Neurochemical research · 2024Article
- Mutation in glutamate transporter homologue GltTk provides insights into pathologic mechanism of episodic ataxia 6.Nature communications · 2023Article
- Article
- Editorial: Combining computational and experimental approaches to characterize ion channels and transporters.Frontiers in physiology · 2023Article
- The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022Review
- Ataxia-linked SLC1A3 mutations alter EAAT1 chloride channel activity and glial regulation of CNS function.The Journal of clinical investigation · 2022Article
- Impedance-Based Phenotypic Readout of Transporter Function: A Case for Glutamate Transporters.Frontiers in pharmacology · 2022Article
- Reconstitution of GABA, Glycine and Glutamate Transporters.Neurochemical research · 2022Review
- Molecular Basis of Coupled Transport and Anion Conduction in Excitatory Amino Acid Transporters.Neurochemical research · 2022Review
- Role of glutamate excitotoxicity and glutamate transporter EAAT2 in epilepsy: Opportunities for novel therapeutics development.Biochemical pharmacology · 2021Review
- Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage.International journal of molecular sciences · 2021Review
- Cellular Physiology and Pathophysiology of EAAT Anion Channels.Frontiers in cellular neuroscience · 2021Review
- Glutamic Acid Transporters: Targets for Neuroprotective Therapies in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- Therapeutic Potential of Sodium Channel Blockers as a Targeted Therapy Approach inFrontiers in neurology · 2021Article
- Glial Chloride Homeostasis Under Transient Ischemic Stress.Frontiers in cellular neuroscience · 2021Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Episodic ataxia type 6 is an inherited neurological condition characterized by combined ataxia and epilepsy. A severe form of this disease with episodes combining ataxia, epilepsy and hemiplegia was recently associated with a proline to arginine substitution at position 290 of the excitatory amino acid transporter 1 in a heterozygous patient. The excitatory amino acid transporter 1 is the predominant glial glutamate transporter in the cerebellum. However, this glutamate transporter also functions as an anion channel and earlier work in heterologous expression systems demonstrated that the mutation impairs the glutamate transport rate, while increasing channel activity. To understand how these changes cause ataxia, we developed a constitutive transgenic mouse model. Transgenic mice display epilepsy, ataxia and cerebellar atrophy and, thus, closely resemble the human disease. We observed increased glutamate-activated chloride efflux in Bergmann glia that triggers the apoptosis of these cells during infancy. The loss of Bergmann glia results in reduced glutamate uptake and impaired neural network formation in the cerebellar cortex. This study shows how gain-of-function of glutamate transporter-associated anion channels causes ataxia through modifying cerebellar development.
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.