Expression of Neuronal Na+/K+-ATPase α Subunit Isoforms in the Mouse Brain Following Genetically Programmed or Behaviourally-induced Oxidative Stress

Lowry, Chloe A.; Golod, Michael; Andrew, R. David; Bennett, Brian M.

doi:10.1016/j.neuroscience.2020.07.009

Cited by 5 publications

(5 citation statements)

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“…In support, the alpha 2 and alpha 3 isoforms are proposed to reduce vulnerability to ischemia compared with alpha 1 [56,103]. Mined data from the Allen Brain Bank [104] indicate that the hypothalamus and the brainstem neurons express a greater proportion of alpha 3 to alpha 1 compared with the higher brain regions of the neocortex, thalamus, striatum, and hippocampus [105]. This may help explain how hypothalamic neurons [106] and brainstem neurons [95] can maintain firing, better resist complete depolarization, and better recover during OGD in contrast to neurons in higher brain regions, which immediately succumb to SD.…”

Section: Na + /K + Atpase Isoforms and Sdmentioning

confidence: 99%

“…This may help explain how hypothalamic neurons [106] and brainstem neurons [95] can maintain firing, better resist complete depolarization, and better recover during OGD in contrast to neurons in higher brain regions, which immediately succumb to SD. Note that the hippocampus displays an intermediate proportion of alpha 3 expression yet is susceptible to SD and ischemic damage, so an elevated neuronal alpha 3 expression does not guarantee increased resistance to ischemia [105]. The lower projection neurons resist SD evoked by OGD or ouabain [107] or by high [K + ] o [108], likely because alpha 3 more efficiently removes higher levels of intracellular Na + .…”

Section: Na + /K + Atpase Isoforms and Sdmentioning

confidence: 99%

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The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

et al. 2022

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Background When a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD. Methods In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na+/K+ pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate. Results We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na+/K+ ATPase elicits SD. Elevated K+ or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling. Conclusions Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory.

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Section: Na + /K + Atpase Isoforms and Sdmentioning

confidence: 99%

Section: Na + /K + Atpase Isoforms and Sdmentioning

confidence: 99%

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

et al. 2022

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“…LP caused by OS can interfere with the transportation of Ca 2+ and increase the intracellular Ca 2+ concentrations via inhibiting the activation of Ca 2+ -pump ATPase. At the same time, the inhibition of Na+/K + -pump ATPase caused by OS can increase the accumulation of Na+and further promote the accumulation of Ca 2+ in cells ( Lowry et al, 2020 ). With the influx of Na + and the alterations of change of osmotic pressure, cytotoxic cellular edema occurs, further promoting intracellular phospholipase activity and intracellular acidosis ( Piao et al, 2011 ).…”

Section: The Pathophysiology Of Spinal Cord Injurymentioning

confidence: 99%

Application of natural antioxidants from traditional Chinese medicine in the treatment of spinal cord injury

Huang

Wang²,

Li³

et al. 2022

Front. Pharmacol.

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Spinal cord injury (SCI) is a devastating central nervous system disease, caused by physical traumas. With the characteristic of high disability rate, catastrophic dysfunction, and enormous burden on the patient’s family, SCI has become a tough neurological problem without efficient treatments. Contemporarily, the pathophysiology of SCI comprises complicated and underlying mechanisms, in which oxidative stress (OS) may play a critical role in contributing to a cascade of secondary injuries. OS substantively leads to ion imbalance, lipid peroxidation, inflammatory cell infiltration, mitochondrial disorder, and neuronal dysfunction. Hence, seeking the therapeutic intervention of alleviating OS and appropriate antioxidants is an essential clinical strategy. Previous studies have reported that traditional Chinese medicine (TCM) has antioxidant, anti-inflammatory, antiapoptotic and neuroprotective effects on alleviating SCI. Notably, the antioxidant effects of some metabolites and compounds of TCM have obtained numerous verifications, suggesting a potential therapeutic strategy for SCI. This review aims at investigating the mechanisms of OS in SCI and highlighting some TCM with antioxidant capacity used in the treatment of SCI.

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“…The interchange of ions taking place in these double strand lipid layers is facilitated by Na + , K + ATPase enzyme that stimulates the entrance and exit of Na + and K + in the cell 13 . ATPase is a membrane protein whose activity in the central nervous system (CNS) is very sensitive to oxidative stress 14 , 15 . Enzymatic activity modification of Na(+)/K(+) ATPase has been reported in anti-cancer agents induced oxidative stress 16 .…”

Section: Introductionmentioning

confidence: 99%

Intake of oligoelements with cytarabine or etoposide alters dopamine levels and oxidative damage in rat brain

Guzmán,

Brizuela,

Herrera

et al. 2024

Sci Rep

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Research on the relationships between oligoelements (OE) and the development of cancer or its prevention is a field that is gaining increasing relevance. The aim was to evaluate OE and their interactions with oncology treatments (cytarabine or etoposide) to determine the effects of this combination on biogenic amines and oxidative stress biomarkers in the brain regions of young Wistar rats. Dopamine (DA), 5-Hydroxyindoleacetic acid (5-Hiaa), Glutathione (Gsh), Tiobarbituric acid reactive substances (TBARS) and Ca+2, Mg+2 ATPase enzyme activity were measured in brain regions tissues using spectrophometric and fluorometric methods previously validated. The combination of oligoelements and cytarabine increased dopamine in the striatum but decreased it in cerebellum/medulla-oblongata, whereas the combination of oligoelements and etoposide reduced lipid peroxidation. These results suggest that supplementation with oligoelements modifies the effects of cytarabine and etoposide by redox pathways, and may become promising therapeutic targets in patients with cancer.

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Expression of Neuronal Na+/K+-ATPase α Subunit Isoforms in the Mouse Brain Following Genetically Programmed or Behaviourally-induced Oxidative Stress

Cited by 5 publications

References 60 publications

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

Application of natural antioxidants from traditional Chinese medicine in the treatment of spinal cord injury

Intake of oligoelements with cytarabine or etoposide alters dopamine levels and oxidative damage in rat brain

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