ArticlePloS one2014
Role of Na,K-ATPase α1 and α2 isoforms in the support of astrocyte glutamate uptake.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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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
34 citing papers in PubMed, 61 citations in OpenAlex.
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- Early onset severe ATP1A2 epileptic encephalopathy: Clinical characteristics and underlying mutations.Epilepsy & behavior : E&B · 2021Article
- Astrocyte deletion of α2-Na/K ATPase triggers episodic motor paralysis in mice via a metabolic pathway.Nature communications · 2020Article
- Regulation of Na/K-ATPase expression by cholesterol: isoform specificity and the molecular mechanism.American journal of physiology. Cell physiology · 2020Article
- Changes in Inflammatory Response, Redox Status and NaNeurotoxicity research · 2020Article
- Glial Cells-The Strategic Targets in Amyotrophic Lateral Sclerosis Treatment.Journal of clinical medicine · 2020Review
- Sodium Fluctuations in Astroglia and Their Potential Impact on Astrocyte Function.Frontiers in physiology · 2020Review
- Physiology of Astroglial Excitability.Function (Oxford, England) · 2020Article
- Glutamate Transporters in Hippocampal LTD/LTP: Not Just Prevention of Excitotoxicity.Frontiers in cellular neuroscience · 2019Review
- A novel ATP1A2 mutation in a patient with hypokalaemic periodic paralysis and CNS symptoms.Brain : a journal of neurology · 2018Article
- Homocysteine Induces Glial Reactivity in Adult Rat Astrocyte Cultures.Molecular neurobiology · 2018Article
Corrections and comments
- Erratum issuedIllarionava, Nina B [corrected to Illarionova, Nina B]
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate released during neuronal activity is cleared from the synaptic space via the astrocytic glutamate/Na(+) co-transporters. This transport is driven by the transmembrane Na(+) gradient mediated by Na,K-ATPase. Astrocytes express two isoforms of the catalytic Na,K-ATPase α subunits; the ubiquitously expressed α1 subunit and the α2 subunit that has a more specific expression profile. In the brain α2 is predominantly expressed in astrocytes. The isoforms differ with regard to Na+ affinity, which is lower for α2. The relative roles of the α1 and α2 isoforms in astrocytes are not well understood. Here we present evidence that the presence of the α2 isoform may contribute to a more efficient restoration of glutamate triggered increases in intracellular sodium concentration [Na(+)]i. Studies were performed on primary astrocytes derived from E17 rat striatum expressing Na,K-ATPase α1 and α2 and the glutamate/Na(+) co-transporter GLAST. Selective inhibition of α2 resulted in a modest increase of [Na(+)]i accompanied by a disproportionately large decrease in uptake of aspartate, an indicator of glutamate uptake. To compare the capacity of α1 and α2 to handle increases in [Na(+)]i triggered by glutamate, primary astrocytes overexpressing either α1 or α2 were used. Exposure to glutamate 200 µM caused a significantly larger increase in [Na(+)]i in α1 than in α2 overexpressing cells, and as a consequence restoration of [Na(+)]i, after glutamate exposure was discontinued, took longer time in α1 than in α2 overexpressing cells. Both α1 and α2 interacted with astrocyte glutamate/Na(+) co-transporters via the 1st intracellular loop.
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