ArticleThe Journal of biological chemistry2013
A specific and essential role for Na,K-ATPase α3 in neurons co-expressing α1 and α3.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed.
- ATP1A3-related neurological disorders: updated insights into clinical heterogeneity, molecular mechanisms and precision therapeutics.Neurogenetics · 2026Review
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- Chronic Administration of Marinobufagenin in Mice Causes Hyperlocomotion and Decrease in Anxiety by Altering Monoamine Turnover Unaccompanied by Motor Deficits or Oxidative Stress.International journal of molecular sciences · 2026Article
- Pathophysiological Roles of Two Intracellular P-Type ATPases: The Cancer-Associated NaInternational journal of molecular sciences · 2026Review
- Pathogenic Variants inNeurology. Genetics · 2025Article
- Spatiotemporal Dynamics of Lateral NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Multistate Kinetic Model of the Sodium-Potassium ATPase.The journal of physical chemistry. B · 2025Article
- Spatio-temporal dynamics of lateral NabioRxiv : the preprint server for biology · 2025Article
- Alternating hemiplegia of childhood associated mutations in Atp1a3 reveal diverse neurological alterations in mice.Neurobiology of disease · 2025Article
- ATP1A3 dysfunction causes motor hyperexcitability and afterhyperpolarization loss in a dystonia model.Brain : a journal of neurology · 2025Article
- Mechanisms mediating effects of cardiotonic steroids in mammalian blood cells.Frontiers in pharmacology · 2025Review
- Phenotype Distinctions in Mice Deficient in the Neuron-Specific α3 Subunit of Na,K-ATPase:eNeuro · 2024Article
- Neuronal autosis is NaCell death & disease · 2024Article
- Oral ATP treatment in alternating hemiplegia of childhood: a case report and review.Frontiers in medicine · 2024Article
- Histological Correlates of Auditory Nerve Injury from Kainic Acid in the Budgerigar (Melopsittacus undulatus).Journal of the Association for Research in Otolaryngology : JARO · 2023Article
- The zebrafish mutanteLife · 2023Article
- NaBiomedicines · 2023Review
- The role ofFrontiers in cellular neuroscience · 2023Review
- The NaeLife · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
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Abstract
Most neurons co-express two catalytic isoforms of Na,K-ATPase, the ubiquitous α1, and the more selectively expressed α3. Although neurological syndromes are associated with α3 mutations, the specific role of this isoform is not completely understood. Here, we used electrophysiological and Na(+) imaging techniques to study the role of α3 in central nervous system neurons expressing both isoforms. Under basal conditions, selective inhibition of α3 using a low concentration of the cardiac glycoside, ouabain, resulted in a modest increase in intracellular Na(+) concentration ([Na(+)](i)) accompanied by membrane potential depolarization. When neurons were challenged with a large rapid increase in [Na(+)](i), similar to what could be expected following suprathreshold neuronal activity, selective inhibition of α3 almost completely abolished the capacity to restore [Na(+)](i) in soma and dendrite. Recordings of Na,K-ATPase specific current supported the notion that when [Na(+)](i) is elevated in the neuron, α3 is the predominant isoform responsible for rapid extrusion of Na(+). Low concentrations of ouabain were also found to disrupt cortical network oscillations, providing further support for the importance of α3 function in the central nervous system. The α isoforms express a well conserved protein kinase A consensus site, which is structurally associated with an Na(+) binding site. Following activation of protein kinase A, both the α3-dependent current and restoration of dendritic [Na(+)](i) were significantly attenuated, indicating that α3 is a target for phosphorylation and may participate in short term regulation of neuronal function.
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