ReviewMolecular neurobiology2016
Glutamate Transporters/Na(+), K(+)-ATPase Involving in the Neuroprotective Effect as a Potential Regulatory Target of Glutamate Uptake.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Osmoregulatory strategies of estuarine fish Scatophagus argus in response to environmental salinity changes.BMC genomics · 2022Article
- Antioxidant and Anticholinesterase Properties of the Aqueous Extract ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Monosodium glutamate induces memory and hepatic dysfunctions in mice: ameliorative role of JobelynToxicological research · 2021Article
- Disruption of Glutamate Release and Uptake-Related Protein Expression After Noise-Induced Synaptopathy in the Cochlea.Frontiers in cell and developmental biology · 2021Article
- Changes in Inflammatory Response, Redox Status and NaNeurotoxicity research · 2020Article
- Transcriptional analysis of renal dopamine-mediated NaBMC genomics · 2019Article
- Valproate and sodium butyrate attenuate manganese-decreased locomotor activity and astrocytic glutamate transporters expression in mice.Neurotoxicology · 2018Article
- The Influence of Na(+), K(+)-ATPase on Glutamate Signaling in Neurodegenerative Diseases and Senescence.Frontiers in physiology · 2016Review
- Cytokine and Growth Factor Activation In Vivo and In Vitro after Spinal Cord Injury.Mediators of inflammation · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glutamate (Glu) transporters GLAST and GLT-1, as the two most important transporters in brain tissue, transport Glu from the extracellular space into the cell protecting against Glu toxicity. Furthermore, GLAST and GLT-1 are sodium-dependent Glu transporters (GluTs) that rely on sodium and potassium gradients generated principally by Na(+), K(+)-ATPase to generate ion gradients that drive Glu uptake. There is an interaction between Na(+), K(+)-ATPase and GluTs to modulate Glu uptake, and Na(+), K(+)-ATPase α, β or γ subunit can be directly coupled to GluTs, co-localizing with GLAST or GLT-1 in vivo to form a macromolecular complex and operate as a functional unit to regulate glutamatergic neurotransmission. Therefore, GluTs/Na(+), K(+)-ATPase may be involved in the neuroprotective effect as a potential regulatory target of Glu uptake in neurodegenerative diseases induced by Glu-mediated neurotoxicity as the final common pathway.
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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.