ArticleNeurochemical research2013
Cell-specific mRNA alterations in Na+, K+-ATPase α and β isoforms and FXYD in mice treated chronically with carbamazepine, an anti-bipolar drug.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- The functions of FXYD family members in human health and disease.Genes & diseases · 2026Review
- Astroglial Serotonin Receptors as the Central Target of Classic Antidepressants.Advances in neurobiology · 2021Article
- How glycogen sustains brain function: A plausible allosteric signaling pathway mediated by glucose phosphates.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Review
- Article
- The Glycoside Oleandrin Reduces Glioma Growth with Direct and Indirect Effects on Tumor Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Glutamate transporter activity promotes enhanced NaThe Journal of physiology · 2016Article
- Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.Frontiers in physiology · 2016Review
- Managing Brain Extracellular K(+) during Neuronal Activity: The Physiological Role of the Na(+)/K(+)-ATPase Subunit Isoforms.Frontiers in physiology · 2016Review
- Role of the Astrocytic Na(+), K(+)-ATPase in K(+) Homeostasis in Brain: K(+) Uptake, Signaling Pathways and Substrate Utilization.Neurochemical research · 2015Review
- Glial pathology in bipolar disorder: potential therapeutic implications.CNS neuroscience & therapeutics · 2015Review
- Ammonium activates ouabain-activated signalling pathway in astrocytes: therapeutic potential of ouabain antagonist.Current neuropharmacology · 2014Article
- Antagonists of the Vasopressin V1 Receptor and of the β(1)-Adrenoceptor Inhibit Cytotoxic Brain Edema in Stroke by Effects on Astrocytes - but the Mechanisms Differ.Current neuropharmacology · 2014Article
- Article
- Signal Transduction in Astrocytes during Chronic or Acute Treatment with Drugs (SSRIs, Antibipolar Drugs, GABA-ergic Drugs, and Benzodiazepines) Ameliorating Mood Disorders.Journal of signal transduction · 2014Review
- Methodological limitations in determining astrocytic gene expression.Frontiers in endocrinology · 2013Review
- When can AQP4 assist transporter-mediated K⁺ uptake?The Journal of general physiology · 2013Article
- Astrocytic and neuronal accumulation of elevated extracellular K(+) with a 2/3 K(+)/Na(+) flux ratio-consequences for energy metabolism, osmolarity and higher brain function.Frontiers in computational neuroscience · 2013Article
Corrections and comments
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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
Evidence accumulating during almost 50 years suggests Na(+), K(+)-ATPase dysfunction in bipolar disorder, a disease treatable with chronic administration of lithium salts, carbamazepine or valproic acid. Three Na(+), K(+)-ATPase α subunits (α1-3) and two β subunits (β1 and β2) are expressed in brain together with the auxiliary protein FXYD7. FXYD7 decreases K(+) affinity, and thus contributes to stimulation of the enzyme at elevated extracellular K(+) concentrations. Na(+), K(+)-ATPase subtype and FXYD7 genes were determined by RT-PCR in mice co-expressing one fluorescent signal with an astrocytic marker or a different fluorescent signal with a neuronal marker and treated for 14 days with carbamazepine. Following fluorescence-activated cell sorting of neurons and astrocytes it was shown that α2 Expression was upregulated in astrocytes and neurons and α1 selectively in neurons, but α3 was unchanged. β1 was upregulated in astrocytes, but not in neurons. β2 was unaffected in astrocytes and absent in neurons. FXYD7 was downregulated specifically in neurons. According to cited literature data these changes should facilitate K(+) uptake in neurons, without compromising preferential uptake in astrocytes at increased extracellular K(+) concentrations. This process seems to be important for K(+) homeostasis of the cellular level of the brain (Xu et al. Neurochem Res E-pub Dec. 12, 2012).
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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.