ReviewFrontiers in physiology2016
Managing Brain Extracellular K(+) during Neuronal Activity: The Physiological Role of the Na(+)/K(+)-ATPase Subunit Isoforms.
Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Effect of ouabain on calcium signaling in rodent brain: A systematic review ofFrontiers in pharmacology · 2022Pooled it
- Cellular and subcellular heterogeneity of astrocytic Na⁺ homeostasis tuning astrocytes into functionally distinct subgroups in the mouse brain.Nature communications · 2026Article
- Influence of extracellular magnesium ions on the functional state and biophysical and structural properties of connexin36 hemichannels.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dravet Syndrome Patient-Derived Neural Cells Present Altered Levels of Potassium, Copper, and Zinc.ACS chemical neuroscience · 2026Article
- Chemogenetic Schwann cell activation impairs early myelination and triggers adult demyelination in the peripheral nervous system.Frontiers in cellular neuroscience · 2026Article
- The Impact of Aquaporin-4 Deletion on KGlia · 2026Article
- Contribution of glial inwardly rectifying potassium (Kir) channels to potassium buffering in insect neural systems.iScience · 2025Article
- Glial Versus Neuronal NaGlia · 2025Article
- Deficient Astrocyte Homeostatic Support Contributes to Brain Impairment in Duchenne Muscular Dystrophy.Neurochemical research · 2025Review
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- Interplay of Neuroinflammation and Epilepsy in Glioblastoma Multiforme: Mechanisms and Therapeutic Implications.Journal of molecular neuroscience : MN · 2025Review
- Small molecule ion channel agonist/antagonist screen reveals seizure suppression via glial Irk2 activation in a Drosophila model of Dup15q syndrome.Neurobiology of disease · 2025Article
- Na,K-ATPase mediated and cardiotonic induced signaling in health and disease.Frontiers in physiology · 2025Review
- The Na+/K+-ATPase generically enables deterministic bursting in class I neurons by shearing the spike-onset bifurcation structure.PLoS computational biology · 2024Article
- Probing intracellular potassium dynamics in neurons with the genetically encoded sensor lc-LysM GEPII 1.0 in vitro and in vivo.Scientific reports · 2024Article
- Alterations in brain fluid physiology during the early stages of development of ischaemic oedema.Fluids and barriers of the CNS · 2024Review
- ALS-like pathology diminishes swelling of spinal astrocytes in the SOD1 animal model.Frontiers in cellular neuroscience · 2024Article
- Evolution of Consciousness.Life (Basel, Switzerland) · 2023Review
- Energy optimisation predicts the capacity of ion buffering in the brain.Biological cybernetics · 2023Article
- Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During neuronal activity in the brain, extracellular K(+) rises and is subsequently removed to prevent a widespread depolarization. One of the key players in regulating extracellular K(+) is the Na(+)/K(+)-ATPase, although the relative involvement and physiological impact of the different subunit isoform compositions of the Na(+)/K(+)-ATPase remain unresolved. The various cell types in the brain serve a certain temporal contribution in the face of network activity; astrocytes respond directly to the immediate release of K(+) from neurons, whereas the neurons themselves become the primary K(+) absorbers as activity ends. The kinetic characteristics of the catalytic α subunit isoforms of the Na(+)/K(+)-ATPase are, partly, determined by the accessory β subunit with which they combine. The isoform combinations expressed by astrocytes and neurons, respectively, appear to be in line with the kinetic characteristics required to fulfill their distinct physiological roles in clearance of K(+) from the extracellular space in the face of neuronal activity. Understanding the nature, impact and effects of the various Na(+)/K(+)-ATPase isoform combinations in K(+) management in the central nervous system might reveal insights into pathological conditions such as epilepsy, migraine, and spreading depolarization following cerebral ischemia. In addition, particular neurological diseases occur as a result of mutations in the α2- (familial hemiplegic migraine type 2) and α3 isoforms (rapid-onset dystonia parkinsonism/alternating hemiplegia of childhood). This review addresses aspects of the Na(+)/K(+)-ATPase in the regulation of extracellular K(+) in the central nervous system as well as the related pathophysiology. Understanding the physiological setting in non-pathological tissue would provide a better understanding of the pathological events occurring during disease.
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